Database : MEDLINE
Search on : Memory and Disorders [Words]
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[PMID]: 29524763
[Au] Autor:Atsak P; Morena M; Schoenmaker C; Tabak E; Oomen CA; Jamil S; Hill MN; Roozendaal B
[Ad] Address:Department of Cognitive Neuroscience, Radboud University Medical Center, 6500 HB Nijmegen, The Netherlands; Donders Institute for Brain, Cognition and Behaviour, Radboud University, 6525 EN Nijmegen, The Netherlands. Electronic address: PirayAtsak@gmail.com.
[Ti] Title:Glucocorticoid-endocannabinoid uncoupling mediates fear suppression deficits after early - Life stress.
[So] Source:Psychoneuroendocrinology;91:41-49, 2018 Feb 21.
[Is] ISSN:1873-3360
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Early-life stress (ELS) creates life-long vulnerability to stress-related anxiety disorders through altering stress and fear systems in the brain. The endocannabinoid system has emerged as an important regulator of the stress response through a crosstalk with the glucocorticoid system, yet whether it plays a role in the persistent effects of ELS remains unanswered. By combining, behavioral, pharmacological and biochemical approaches in adult male rats, we examined the impact of ELS on the regulation of endocannabinoid function by stress and glucocorticoids. We employed a postnatal limited-nesting/bedding induced ELS between postnatal days 2-9 in rats. Exposure to postnatal ELS compromised the ability of both acute stress and glucocorticoid administration to mobilize the endocannabinoid ligand 2-arachidonoyl glycerol (2-AG) in the hippocampus of adult male rats. These findings suggest that ELS compromises the coupling of the glucocorticoid and endocannabinoid systems in the hippocampus. Since 2-AG signaling is essential in mediating glucocorticoid-induced suppression of fear recall, we further examined the impact of ELS on the ability of glucocorticoids to suppress fear memory recall. While ELS did not affect normative fear recall, it impaired the ability of glucocorticoids to dampen fear recall. Notably, bypassing glucocorticoids and directly amplifying hippocampal 2-AG signaling with a monoacyl glycerol lipase inhibitor produced a suppression of fear memory recall in animals exposed to ELS. These findings suggest that ELS results in an uncoupling of glucocorticoid-endocannabinoid signaling in the hippocampus, which, in turn, relates to alterations in stress regulation of memory recall. These data provide compelling evidence that ELS-induced deficits in the glucocorticoid-endocannabinoid coupling following stress could predispose susceptibility to stress-related psychopathology.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 98560 MEDLINE  
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[PMID]: 29524638
[Au] Autor:Bian C; Huang Y; Zhu H; Zhao Y; Zhao J; Zhang J
[Ad] Address:Department of Military Psychology, College of Psychology, Third Military Medical University, Chongqing 400038, China; Department of Neurobiology, Third Military Medical University, Chongqing 400038, China.
[Ti] Title:Steroid receptor coactivator-1 knockdown decreases synaptic plasticity and impairs spatial memory in the hippocampus of mice.
[So] Source:Neuroscience;, 2018 Mar 07.
[Is] ISSN:1873-7544
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Steroids have been demonstrated to play profound roles in the regulation of hippocampal function by acting on their receptors, which need coactivators for their transcriptional activities. Previous studies have shown that steroid receptor coactivator-1 (SRC-1) is the predominant coactivator in the hippocampus, but its exact role and the underlying mechanisms remain unclear. In this study, we constructed SRC-1 RNA interference lentiviruses, injected them into the hippocampus of male mice, and then examined the changes in the expression of selected synaptic proteins, CA1 synapse density, postsynaptic density (PSD) thickness, and in vivo long-term potentiation (LTP). Spatial learning and memory behavior changes were investigated using the Morris water maze. We then transfected the lentiviruses into cultured hippocampal cells and examined the changes in synaptic protein and phospho-CREB (pCREB) expression. The in vivo results showed that SRC-1 knockdown significantly decreased the expression of synaptic proteins and CA1 synapse density as well as PSD thickness; SRC-1 knockdown also significantly impaired in vivo LTP and disrupted spatial learning and memory. The in vitro results showed that while the expression of synaptic proteins was significantly decreased by SRC-1 knockdown, pCREB expression was also significantly decreased. The above results suggest a pivotal role of SRC-1 in the regulation of hippocampal synaptic plasticity and spatial learning and memory, strongly indicating SRC-1 may serve as a novel therapeutic target for hippocampus-dependent memory disorders.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 98560 MEDLINE  
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[PMID]: 29466709
[Au] Autor:Mandal A; Prabhavalkar KS; Bhatt LK
[Ad] Address:Department of Pharmacology, SVKM's Dr Bhanuben Nanavati College of Pharmacy, Vile Parle (W), Mumbai, India.
[Ti] Title:Gastrointestinal hormones in regulation of memory.
[So] Source:Peptides;102:16-25, 2018 Feb 18.
[Is] ISSN:1873-5169
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The connection between the gastrointestinal hormones and the brain has been established many years ago. This relation is termed the gut-brain axis (GBA). The GBA is a bidirectional communication which not only regulates gastrointestinal homeostasis but is also linked with higher emotional and cognitive functions. Hypothalamus plays a critical role in the regulation of energy metabolism, nutrient partitioning and control of feeding behaviors. Various gut hormones are released inside the gastrointestinal tract on food intake. These hormones act peripherally and influence the different responses of the tissues to the food intake, but do also have effects on the brain. The hypothalamus, in turn, integrates visceral function with limbic system structures such as hippocampus, amygdala, and cerebral cortex. The hippocampus has been known for its involvement in the cognitive function and the modulation of synaptic plasticity. This review aims to establish the role of various gut hormones in learning and memory, through the interaction of various receptors in the hippocampus. Understanding their role in memory can also aid in finding novel therapeutic strategies for the treatment of the neurological disorders associated with memory dysfunctions.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  4 / 98560 MEDLINE  
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[PMID]: 29408968
[Au] Autor:Qi S; Yang X; Zhao L; Calhoun VD; Perrone-Bizzozero N; Liu S; Jiang R; Jiang T; Sui J; Ma X
[Ad] Address:Brainnetome Center and National Laboratory of Pattern Recognition, Institute of Automation, Chinese Academy of Sciences, China.
[Ti] Title:MicroRNA132 associated multimodal neuroimaging patterns in unmedicated major depressive disorder.
[So] Source:Brain;, 2018 Feb 02.
[Is] ISSN:1460-2156
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:There is compelling evidence that epigenetic factors contribute to the manifestation of depression, in which microRNA132 (miR-132) is suggested to play a pivotal role in the pathogenesis and neuronal mechanisms underlying the symptoms of depression. Additionally, several depression-associated genes [MECP2, ARHGAP32 (p250GAP), CREB, and period genes] were experimentally validated as miR-132 targets. However, most studies regarding miR-132 in major depressive disorder are based on post-mortem, animal models or genetic comparisons. This work will be the first attempt to investigate how miR-132 dysregulation may impact covariation of multimodal brain imaging data in 81 unmedicated major depressive patients and 123 demographically-matched healthy controls, as well as in a medication-naïve subset of major depressive patients. MiR-132 values in blood (patients > controls) was used as a prior reference to guide fusion of three MRI features: fractional amplitude of low frequency fluctuations, grey matter volume, and fractional anisotropy. The multimodal components correlated with miR-132 also show significant group difference in loadings. Results indicate that (i) higher miR-132 levels in major depressive disorder are associated with both lower fractional amplitude of low frequency fluctuations and lower grey matter volume in fronto-limbic network; and (ii) the identified brain regions linked with increased miR-132 levels were also associated with poorer cognitive performance in attention and executive function. Using a data-driven, supervised-learning method, we determined that miR-132 dysregulation in major depressive disorder is associated with multi-facets of brain function and structure in fronto-limbic network (the key network for emotional regulation and memory), which deepens our understanding of how miR-132 dysregulation in major depressive disorders contribute to the loss of specific brain areas and is linked to relevant cognitive impairments.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher
[do] DOI:10.1093/brain/awx366

  5 / 98560 MEDLINE  
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[PMID]: 29206893
[Au] Autor:Hoche F; Guell X; Vangel MG; Sherman JC; Schmahmann JD
[Ad] Address:Ataxia Unit, Cognitive Behavioral Neurology Unit, Laboratory for Neuroanatomy and Cerebellar Neurobiology, Department of Neurology Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
[Ti] Title:The cerebellar cognitive affective/Schmahmann syndrome scale.
[So] Source:Brain;141(1):248-270, 2018 Jan 01.
[Is] ISSN:1460-2156
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Cerebellar cognitive affective syndrome (CCAS; Schmahmann's syndrome) is characterized by deficits in executive function, linguistic processing, spatial cognition, and affect regulation. Diagnosis currently relies on detailed neuropsychological testing. The aim of this study was to develop an office or bedside cognitive screen to help identify CCAS in cerebellar patients. Secondary objectives were to evaluate whether available brief tests of mental function detect cognitive impairment in cerebellar patients, whether cognitive performance is different in patients with isolated cerebellar lesions versus complex cerebrocerebellar pathology, and whether there are cognitive deficits that should raise red flags about extra-cerebellar pathology. Comprehensive standard neuropsychological tests, experimental measures and clinical rating scales were administered to 77 patients with cerebellar disease-36 isolated cerebellar degeneration or injury, and 41 complex cerebrocerebellar pathology-and to healthy matched controls. Tests that differentiated patients from controls were used to develop a screening instrument that includes the cardinal elements of CCAS. We validated this new scale in a new cohort of 39 cerebellar patients and 55 healthy controls. We confirm the defining features of CCAS using neuropsychological measures. Deficits in executive function were most pronounced for working memory, mental flexibility, and abstract reasoning. Language deficits included verb for noun generation and phonemic > semantic fluency. Visual spatial function was degraded in performance and interpretation of visual stimuli. Neuropsychiatric features included impairments in attentional control, emotional control, psychosis spectrum disorders and social skill set. From these results, we derived a 10-item scale providing total raw score, cut-offs for each test, and pass/fail criteria that determined 'possible' (one test failed), 'probable' (two tests failed), and 'definite' CCAS (three tests failed). When applied to the exploratory cohort, and administered to the validation cohort, the CCAS/Schmahmann scale identified sensitivity and selectivity, respectively as possible exploratory cohort: 85%/74%, validation cohort: 95%/78%; probable exploratory cohort: 58%/94%, validation cohort: 82%/93%; and definite exploratory cohort: 48%/100%, validation cohort: 46%/100%. In patients in the exploratory cohort, Mini-Mental State Examination and Montreal Cognitive Assessment scores were within normal range. Complex cerebrocerebellar disease patients were impaired on similarities in comparison to isolated cerebellar disease. Inability to recall words from multiple choice occurred only in patients with extra-cerebellar disease. The CCAS/Schmahmann syndrome scale is useful for expedited clinical assessment of CCAS in patients with cerebellar disorders.awx317media15678692096001.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1093/brain/awx317

  6 / 98560 MEDLINE  
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[PMID]: 29203121
[Au] Autor:Korol DL; Wang W
[Ad] Address:Department of Biology, Syracuse University, Syracuse, NY 13244, United States. Electronic address: dlkorol@syr.edu.
[Ti] Title:Using a memory systems lens to view the effects of estrogens on cognition: Implications for human health.
[So] Source:Physiol Behav;187:67-78, 2018 Apr 01.
[Is] ISSN:1873-507X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Understanding the organizing and activating effects of gonadal steroids on adult physiology can guide insight into sex differences in and hormonal influences on health and disease, ranging from diabetes and other metabolic disorders, emotion and stress regulation, substance abuse, pain perception, immune function and inflammation, to cognitive function and dysfunction accompanying neurological disorders. Because the brain is highly sensitive to many forms of estrogens, it is not surprising that many adult behaviors, including cognitive function, are modulated by estrogens. Estrogens are known for their facilitating effects on learning and memory, but it is becoming increasingly clear that they also can impair learning and memory of some classes of tasks and may do so through direct actions on specific neural systems. This review takes a multiple memory systems approach to understanding how estrogens can at the same time enhance hippocampus-sensitive place learning and impair striatum-sensitive response learning by exploring the role estrogen receptor signaling may play in the opposing cognitive effects of estrogens. Accumulating evidence suggests that neither receptor subtype nor the timing of treatment, i.e. rapid vs slow, explain the bidirectional effects of estrogens on different types of learning. New findings pointing to neural metabolism and the provision of energy substrates by astrocytes as a candidate mechanism for cognitive enhancement and impairment are discussed.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review

  7 / 98560 MEDLINE  
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[PMID]: 28466270
[Au] Autor:Xu J; Kurup P; Nairn AC; Lombroso PJ
[Ad] Address:Child Study Center, Yale University School of Medicine, New Haven, USA.
[Ti] Title:Synaptic NMDA Receptor Activation Induces Ubiquitination and Degradation of STEP .
[So] Source:Mol Neurobiol;55(4):3096-3111, 2018 Apr.
[Is] ISSN:1559-1182
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:NMDA receptor signaling is critical for the development of synaptic plasticity, learning, and memory, and dysregulation of NMDAR signaling is implicated in a number of neurological disorders including schizophrenia (SZ). Previous work has demonstrated that the STriatal-Enriched protein tyrosine Phosphatase 61 kDa (STEP ) is elevated in human SZ postmortem cortical samples and after administration of psychotomimetics to cultures or mice. Here, we report that activation of synaptic NMDAR by bicuculline or D-serine results in the ubiquitination and proteasomal degradation of STEP , and increased surface localization of GluN1/GluN2B receptors. Moreover, bicuculline or D-serine treatments rescue the motor and cognitive deficits in MK-801-treated mice and reduce STEP in mouse frontal cortex. These results suggest that STEP may contribute to the therapeutic effects of D-serine.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1705
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1007/s12035-017-0555-x

  8 / 98560 MEDLINE  
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[PMID]: 29523431
[Au] Autor:Osler M; Rozing MP; Christensen GT; Andersen PK; Jørgensen MB
[Ad] Address:Center for Clinical Research and Prevention, Bispebjerg and Frederiksberg Hospitals, Frederiksberg, Denmark; Department of Public Health, University of Copenhagen, Copenhagen, Denmark; Danish Ageing Research Center, Department of Public Health, University of Southern Denmark, Denmark. Electronic add
[Ti] Title:Electroconvulsive therapy and risk of dementia in patients with affective disorders: a cohort study.
[So] Source:Lancet Psychiatry;, 2018 Mar 06.
[Is] ISSN:2215-0374
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Electroconvulsive therapy (ECT) is the most effective treatment for severe episodes of mood disorders. Temporary memory loss is a common side-effect, but ongoing discussions exist regarding potential long-term adverse cognitive outcomes. Only a few studies have examined the frequency of dementia in patients after ECT. The aim of this study was to examine the association between ECT and risk of subsequent dementia in patients with a first-time hospital diagnosis of affective disorder. METHODS: We did a cohort study of patients aged 10 years and older in Denmark with a first-time hospital contact for an affective disorder from Jan 1, 2005, through Dec 31, 2015, identified in the Danish National Patient Registry with ICD-10 codes F30.0 to F39.9. From the registry we retrieved information on all ECTs registered for patients and followed up patients for incidental dementia (defined by hospital discharge diagnoses or acetylcholinesterase inhibitor use) until Oct 31, 2016. We examined the association between ECT and dementia using Cox regression analyses with multiple adjustments and propensity-score matching on sociodemographic and clinical variables. FINDINGS: Of 168 015 patients included in the study, 5901 (3·5%) patients had at least one ECT. During the median follow-up of 4·9 years (IQR 2·4-7·8) and 872 874 person years, the number of patients who developed dementia was 111 (0·1%) of 99 045 patients aged 10-49 years, 965 (2·7%) of 35 945 aged 50-69 years, and 4128 (12·5%) of 33 025 aged 70-108 years. 217 (3·6%) of the 5901 patients treated with ECT developed dementia, whereas of 162 114 patients not treated with ECT 4987 (3·1%) developed dementia. The corresponding incidences were 70·4 cases per 10 000 person-years (95% CI 61·6-80·5) and 59·2 per 10 000 person-years (57·6-60·8). In patients younger than 50 years and 50-69 years, ECT was not associated with a risk of dementia compared with age-matched patients who were not given ECT (age-adjusted hazard ratio [HR] 1·51, 95% CI 0·67-3·46, p=0·32; and 1·15, 0·91-1·47, p=0·22, respectively). In patients aged 70 years and older, ECT was associated with a decreased rate of dementia (0·68, 95% CI 0·58-0·80; p<0·0001), but in the propensity-score matched sample the HR was attenuated (0·77, 0·59-1·00; p=0·062). 31 754 patients (17·6%) died during follow-up (mortality rate per 1000 person-years 35·7, 95% CI 35·3-36·2) and supplementary analyses suggested that the risk of dementia, taking the competing mortality risk into account, was not significantly associated with ECT (subdistribution HR 0·98, 95% CI 0·76-1·26; p=0·24). INTERPRETATION: ECT was not associated with risk of incidental dementia in patients with affective disorders after correcting for the potential effect of patient selection or competing mortality. The findings from this study support the continued use of ECT in patients with severe episodes of mood disorders, including those who are elderly. FUNDING: Danish Council for Independent Research, Danish Medical Research Council, the Velux Foundation, the Jascha Foundation, and the Doctor Sofus Carl Emil Friis and Olga Doris Friis grant.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  9 / 98560 MEDLINE  
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[PMID]: 29522943
[Au] Autor:Yamamuro K; Kimoto S; Iida J; Kishimoto N; Tanaka S; Toritsuka M; Ikawa D; Yamashita Y; Ota T; Makinodan M; Yoshino H; Kishimoto T
[Ad] Address:Department of Psychiatry, Nara Medical University School of Medicine, Kashihara, Japan. Electronic address: muro@naramed-u.ac.jp.
[Ti] Title:Distinct patterns of blood oxygenation in the prefrontal cortex in clinical phenotypes of schizophrenia and bipolar disorder.
[So] Source:J Affect Disord;234:45-53, 2018 Feb 27.
[Is] ISSN:1573-2517
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:BACKGROUND: Schizophrenia (SZ) and bipolar disorder (BD) are characterized by different clinical symptoms, and have previously been considered as categorically separate. However, several lines of evidence controversially suggest that these two disorders may run on a continuum. While it is therefore important to evaluate the subtle differences between SZ and BD, few studies have investigated the difference of brain functioning between the two by focusing on the common symptoms of cognitive functioning and impulsivity, rather than positive/negative and mood symptoms. Recent developments in near-infrared spectroscopy (NIRS) technology have enabled noninvasive assessment of brain function in people with psychiatric disorders. METHODS: Near-infrared spectroscopy (NIRS) using 24-channels was conducted during the verbal fluency task (VFT) and Stroop color-word task (SCWT) in 38 patients diagnosed with SZ, 34 patients with BD, and 26 age- and sex-matched healthy controls. RESULTS: Oxyhemoglobin changes in the prefrontal cortex (PFC) were significantly lower particularly in the SZ compared to control group during the VFT. On the other hand, these were significantly lower particularly in the BD and SZ group to control group during the SCWT. Regression analysis showed that hemodynamic changes were significantly correlated with verbal memory and impulsivity in both disorders. CONCLUSION: These findings suggest that different hemodynamic responses in the prefrontal cortex might reflect cognitive functioning and impulsivity, providing a greater insight into SZ and BD pathophysiology.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  10 / 98560 MEDLINE  
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[PMID]: 29522770
[Au] Autor:Rishitha N; Muthuraman A
[Ad] Address:Department of Pharmacology, JSS College of Pharmacy, JSS Academy of Higher Education and Research, Mysuru 570 015, Karnataka, India.
[Ti] Title:Therapeutic evaluation of solid lipid nanoparticle of quercetin in pentylenetetrazole induced cognitive impairment of zebrafish.
[So] Source:Life Sci;, 2018 Mar 06.
[Is] ISSN:1879-0631
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:BACKGROUND: Quercetin is a major flavonoid in various plants. It possesses the multiple pharmacological actions like vascular integrity and regulatory action of the blood-brain barrier. AIMS: The present study is focused on evaluating the role of solid lipid nanoparticle of quercetin in pentylenetetrazole (PTZ) induced cognitive impairment of Danio rerio species. MAIN METHODS: The memory impairment of zebrafish was induced by exposing of PTZ in 7.5 mM solution. The pretreatment of solid lipid nanoparticle of quercetin (SLN-Q; 5 and 10 mg/kg) was administered by single intraperitoneal (i.p.) injection. The reference control i.e., donepezil (10 mg/kg) was administered by single intraperitoneal (i.p.) injection. The learning and memory levels were evaluated with different tests like light and dark chamber test; partition preference test; and three (horizontal) compartment tests. In addition, the PTZ induced biochemical changes such as acetylcholinesterase activity, lipid peroxidation, and reduced glutathione levels were assessed in the brain of zebrafish. KEY FINDINGS: The solid lipid nanoparticle of quercetin found to possess the attenuating effect in PTZ induced neurocognitive impairments along with amelioration of biochemical changes. This effect is similar to that of donepezil pretreated group. SIGNIFICANCE: Therefore, this solid lipid nanoparticle of quercetin can be used as future nanomedicine for various neurodegenerative disorders like Alzheimer and Parkinson disorders due to its potential anti-oxidative, anti-lipid peroxidative and acetylcholinesterase inhibitory actions.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher


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