The Nathan Kline Institute
The Nathan Kline Institute
Manseau M.W.,New York University |
Rajparia A.,New York University |
Joseph A.,The Nathan Kline Institute |
Azarchi S.,New York University |
And 3 more authors.
Substance Use and Misuse | Year: 2017
Background: Increasing reports of synthetic cannabinoid (SC)-related adverse events have largely comprised case reports and analyses of calls to poison control centers. Existing studies have also mostly involved white male populations. Objectives: The purpose of this study is to systematically describe clinical characteristics of SC use in a relatively large, diverse, urban sample presenting to a psychiatric emergency setting. Methods: SC users (n = 110) were identified by reviewing charts (n = 948) from the psychiatric emergency service of a large, urban public hospital in the United States for November 2014, which was randomly selected from the 12 months of that year. Sociodemographic data were collected from administrative databases and clinical data were collected from the electronic medical record. Results: SC users were mostly non-white (90.0%) males (95.5%), who were likely to be police-involved (34.5%) and homeless (84.5%). SC users also had significant and often pre-existing psychiatric and substance use comorbidity, including acute psychotic symptoms (70.0%), more than one comorbid psychiatric diagnosis (31.8%) and primary psychotic disorder diagnosis (40.0%), past psychiatric visits to the hospital (70.9%), comorbid substance use (62.7%), agitation requiring intervention (22.7%), and the need for extended psychiatric observation (15.5%) and inpatient admission (34.5%). Relatively limited medical complications were identified. Conclusions/Importance: In this sample, SC use affected a sociodemographically disadvantaged and mentally ill population, likely exacerbating existing psychiatric problems. This is one of the only studies to systematically examine the clinical effects of SC use in a significant clinical sample, and the first study in an urban, racial/ethnic minority, and vulnerable sample. © 2017 Taylor & Francis Group, LLC
Chen K.,Banner Alzheimers Institute and Banner Good Samaritan Center |
Chen K.,Arizona State University |
Langbaum J.B.S.,Banner Alzheimers Institute and Banner Good Samaritan Center |
Fleisher A.S.,Banner Alzheimers Institute and Banner Good Samaritan Center |
And 17 more authors.
NeuroImage | Year: 2010
Alzheimer's disease (AD) is characterized by specific and progressive reductions in fluorodeoxyglucose positron emission tomography (FDG PET) measurements of the cerebral metabolic rate for glucose (CMRgl), some of which may precede the onset of symptoms. In this report, we describe twelve-month CMRgl declines in 69 probable AD patients, 154 amnestic mild cognitive impairment (MCI) patients, and 79 cognitively normal controls (NCs) from the AD Neuroimaging Initiative (ADNI) using statistical parametric mapping (SPM). We introduce the use of an empirically pre-defined statistical region-of-interest (sROI) to characterize CMRgl declines with optimal power and freedom from multiple comparisons, and we estimate the number of patients needed to characterize AD-slowing treatment effects in multi-center randomized clinical trials (RCTs). The AD and MCI groups each had significant twelve-month CMRgl declines bilaterally in posterior cingulate, medial and lateral parietal, medial and lateral temporal, frontal and occipital cortex, which were significantly greater than those in the NC group and correlated with measures of clinical decline. Using sROIs defined based on training sets of baseline and follow-up images to assess CMRgl declines in independent test sets from each patient group, we estimate the need for 66 AD patients or 217 MCI patients per treatment group to detect a 25% AD-slowing treatment effect in a twelve-month, multi-center RCT with 80% power and two-tailed alpha=0.05, roughly one-tenth the number of the patients needed to study MCI patients using clinical endpoints. Our findings support the use of FDG PET, brain-mapping algorithms and empirically pre-defined sROIs in RCTs of AD-slowing treatments. © 2010 Elsevier Inc.
Yang J.,New York Medical College |
Harte-Hargrove L.C.,The Nathan Kline Institute |
Siao C.-J.,New York Medical College |
Marinic T.,New York Medical College |
And 11 more authors.
Cell Reports | Year: 2014
Experience-dependent plasticity shapes postnatal development of neural circuits, but the mechanisms that refine dendritic arbors, remodel spines, and impair synaptic activity are poorly understood. Mature brain-derived neurotrophic factor (BDNF) modulates neuronal morphology and synaptic plasticity, including long-term potentiation (LTP) via TrkB activation. BDNF is initially translated as proBDNF, which binds p75NTR. In vitro, recombinant proBDNF modulates neuronal structure and alters hippocampal long-term plasticity, but the actions of endogenously expressed proBDNF are unclear. Therefore, we generated a cleavage-resistant probdnf knockin mouse. Our results demonstrate that proBDNF negatively regulates hippocampal dendritic complexity and spine density through p75NTR. Hippocampal slices from probdnf mice exhibit depressed synaptic transmission, impaired LTP, and enhanced long-term depression (LTD) in area CA1. These results suggest that proBDNF acts in vivo as a biologically active factor that regulates hippocampal structure, synaptic transmission, and plasticity, effects that are distinct from those of mature BDNF. © 2014 The Authors.
PubMed | Sloan Kettering Cancer Center, The Nathan Kline Institute, Brown University, New York Medical College and New York University
Type: Journal Article | Journal: Cell reports | Year: 2014
Experience-dependent plasticity shapes postnatal development of neural circuits, but the mechanisms that refine dendritic arbors, remodel spines, and impair synaptic activity are poorly understood. Mature brain-derived neurotrophic factor (BDNF) modulates neuronal morphology and synaptic plasticity, including long-term potentiation (LTP) via TrkB activation. BDNF is initially translated as proBDNF, which binds p75(NTR). Invitro, recombinant proBDNF modulates neuronal structure and alters hippocampal long-term plasticity, but the actions ofendogenously expressed proBDNF are unclear. Therefore, we generated a cleavage-resistant probdnf knockin mouse. Our results demonstrate that proBDNF negatively regulates hippocampal dendritic complexity and spine density through p75(NTR). Hippocampal slices from probdnf mice exhibit depressed synaptic transmission, impaired LTP, and enhanced long-term depression (LTD) in area CA1. These results suggest that proBDNF acts invivo as a biologically active factor that regulates hippocampal structure, synaptic transmission, and plasticity, effects that are distinct from those of mature BDNF.
PubMed | The Nathan Kline Institute, Beth Israel Deaconess Medical Center and Cedars Sinai Medical Center
Type: Journal Article | Journal: Journal of Parkinson's disease | Year: 2016
Stimulation of the subthalamic nuclei (STN) is an effective treatment for Parkinsons disease, but complaints of speech difficulties after surgery have been difficult to quantify. Speech measures do not convincingly account for such reports.This study examined STN stimulation effects on vowel production, in order to probe whether DBS affects articulatory posturing. The objective was to compare positioning during the initiation phase with the steady prolongation phase by measuring vowel spaces for three corner vowels at these two time frames.Vowel space was measured over the initial 0.25sec of sustained productions of high front (/i/), high back (/u/) and low vowels (/a/), and again during a 2sec segment at the midpoint. Eight right-handed male subjects with bilateral STN stimulation and seven age-matched male controls were studied based on their participation in a larger study that included functional imaging. Mean values: age=574.6 yrs; PD duration=12.32.7 yrs; duration of DBS=25.621.2 mos, and UPDRS III speech score=1.60.7. STN subjects were studied off medication at their therapeutic DBS settings and again with their stimulators off, counter-balanced order.Vowel space was larger in the initiation phase compared to the midpoint for both the control and the STN subjects off stimulation. With stimulation on, however, the initial vowel space was significantly reduced to the area measured at the mid-point. For the three vowels, the acoustics were differentially affected, in accordance with expected effects of front versus back position in the vocal tract.STN stimulation appears to constrain initial articulatory gestures for vowel production, raising the possibility that articulatory positions normally used in speech are similarly constrained.
McCloskey D.P.,CUNY - College of Staten Island |
Scharfman H.E.,The Nathan Kline Institute |
Scharfman H.E.,New York University
Epilepsy Research | Year: 2011
Rat hippocampal area CA3 pyramidal cells synchronously discharge in rhythmic bursts of action potentials after acute disinhibition or convulsant treatment in vitro. These burst discharges resemble epileptiform activity, and are of interest because they may shed light on mechanisms underlying limbic seizures. However, few studies have examined CA3 burst discharges in an animal model of epilepsy, because a period of prolonged, severe seizures (status epilepticus) is often used to induce the epileptic state, which can lead to extensive neuronal loss in CA3. Therefore, the severity of pilocarpine-induced status epilepticus was decreased with anticonvulsant treatment to reduce damage. Rhythmic burst discharges were recorded in the majority of slices from these animals, between two weeks and nine months after status epilepticus. The incidence and amplitude of bursts progressively increased with time after status, even after spontaneous behavioral seizures had begun. The results suggest that modifying the pilocarpine models of temporal lobe epilepsy to reduce neuronal loss leads to robust network synchronization in area CA3. The finding that these bursts increase long after spontaneous behavioral seizures begin supports previous arguments that temporal lobe epilepsy exhibits progressive pathophysiology. © 2011 Elsevier B.V.
Joseph A.M.,The Nathan Kline Institute |
Manseau M.W.,New York University |
Lalane M.,New York University |
Rajparia A.,New York University |
Lewis C.F.,New York University
American Journal of Drug and Alcohol Abuse | Year: 2016
Background: Growing evidence of adverse outcomes following synthetic cannabinoid use has engendered interest into populations at risk. The existing literature reports that synthetic cannabinoid use is predominant among young, white males. However, reports from local Departments of Health have found contrary evidence, showing that synthetic cannabinoid use is prevalent in populations other than those of young, white men. Objectives: This study sought to examine sociodemographic characteristics associated with self-reported synthetic cannabinoid use among a clinical psychiatric population within a public hospital in New York City. Methods: A cross-sectional medical record review was conducted on synthetic cannabinoid users and non-users in an emergency psychiatric setting. A total of 948 patients who presented at the emergency psychiatric setting in 2014 were included in this sample, 110 (11.6%) of whom were synthetic cannabinoid users. Logistic regressions were used to determine the sociodemographic correlates of synthetic cannabinoid use. Results: The most prominent correlate of synthetic cannabinoid use was homelessness/residing in a shelter during time of treatment (AOR = 17.77, 95% CI = 9.74–32.5). Male (AOR = 5.37, 95% CI = 2.04–14.1), non-white (AOR = 2.74, 95% CI = 1.36–5.54), and younger age (AOR = .961, 95% CI = .940–.980) were also significant correlates of synthetic cannabinoid use. Conclusion: Synthetic cannabinoid use among the homeless and mentally ill is a growing public health concern, representing a population with unique clinical and social needs. Areas and populations with high rates of homelessness should be targeted for synthetic cannabinoid prevention and treatment efforts, particularly in urban and racial/ethnic minority communities. © 2016 Research Foundation for Mental Hygiene, Inc.
Badalamenti A.F.,The Nathan Kline Institute
Journal of Religion and Health | Year: 2013
This paper develops an integration of psychoanalytic and wisdom tradition concepts to answer the question as to why nature does not turn off neurosis, The proposed answer is that nature wants a person to exploit the neurosis for two gains, one being the increase in adaptive capacity resulting from releasing it and the second involving the difficulty in the release itself, the latter related to gains proffered by the world's wisdom traditions. These see a movement from the psyche's creation by passive, unconscious means of finite promise rooted in parental love to creation by active, consciously chosen means of unlimited promise involving a direct relationship with nature and the Cosmos. © 2011 Springer Science+Business Media, LLC.
PubMed | The Nathan Kline Institute
Type: Journal Article | Journal: Journal of religion and health | Year: 2013
This paper develops an integration of psychoanalytic and wisdom tradition concepts to answer the question as to why nature does not turn off neurosis, The proposed answer is that nature wants a person to exploit the neurosis for two gains, one being the increase in adaptive capacity resulting from releasing it and the second involving the difficulty in the release itself, the latter related to gains proffered by the worlds wisdom traditions. These see a movement from the psyches creation by passive, unconscious means of finite promise rooted in parental love to creation by active, consciously chosen means of unlimited promise involving a direct relationship with nature and the Cosmos.
PubMed | The Nathan Kline Institute
Type: | Journal: Epilepsia | Year: 2012
The dentate gyrus is one of two main areas of the mammalian brain where neurons are born throughout adulthood, a phenomenon called postnatal neurogenesis. Most of the neurons that are generated are granule cells (GCs), the major principal cell type in the dentate gyrus. Some adult-born granule cells develop in ectopic locations, such as the dentate hilus. The generation of hilar ectopic granule cells (HEGCs) is greatly increased in several animal models of epilepsy and has also been demonstrated in surgical specimens from patients with intractable temporal lobe epilepsy (TLE). Herein we review the results of our quantitative neuroanatomic analysis of HEGCs that were filled with Neurobiotin following electrophysiologic characterization in hippocampal slices. The data suggest that two types of HEGCs exist, based on a proximal or distal location of the cell body relative to the granule cell layer, and based on the location of most of the dendrites, in the molecular layer or hilus. Three-dimensional reconstruction revealed that the dendrites of distal HEGCs can extend along the transverse and longitudinal axis of the hippocampus. Analysis of axons demonstrated that HEGCs have projections that contribute to the normal mossy fiber innervation of CA3 as well as the abnormal sprouted fibers in the inner molecular layer of epileptic rodents (mossy fiber sprouting). These data support the idea that HEGCs could function as a hub cell in the dentate gyrus and play a critical role in network excitability.