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Search on : Pick and Disease and of and the and Brain [Words]
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[PMID]: 29508660
[Au] Autor:Caplan A; Marx G; Elofson J; Lis C; Grinberg L; Miller B; Rosen H
[Ad] Address:a Memory and Aging Center , University of California San Francisco , San Francisco , CA , USA.
[Ti] Title:A case of semantic variant primary progressive aphasia with Pick's pathology.
[So] Source:Neurocase;:1-5, 2018 Mar 06.
[Is] ISSN:1465-3656
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Neurodegenerative diseases are caused by aggregation of specific proteins that catalyze a cascade of changes that ultimately lead to neurodegeneration. This concept guides current diagnostic approaches, as well as clinical trials, that focus on detecting or removing amyloid or tau from the brain. The semantic variant of primary progressive aphasia (svPPA), a clinical syndrome associated with frontotemporal lobar degeneration (FTLD) pathology, is usually associated with the molecular pathology TDP-C, but there are cases with TDP-B and Pick's disease. The existing literature on the clinical differentiation of these pathologies is limited. Here, we present a case study, in conjunction with a cross-sectional voxel-based morphometry (VBM), to elucidate the clinical and imaging features of a patient with svPPA due to Pick's disease.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:Publisher
[do] DOI:10.1080/13554794.2018.1447134

  2 / 2401 MEDLINE  
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[PMID]: 29497113
[Au] Autor:Alam MS; Cooper B; Farris JD; Haldar K
[Ad] Address:Boler-Parseghian Center for Rare and Neglected Diseases, University of Notre Dame, Notre Dame, IN, 46556, USA.
[Ti] Title:Tolerance of chronic HDACi treatment for neurological, visceral and lung Niemann-Pick Type C disease in mice.
[So] Source:Sci Rep;8(1):3875, 2018 Mar 01.
[Is] ISSN:2045-2322
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Histone deacetylase (HDAC) inhibitors are of significant interest as drugs. However, their use to treat neurological disorders has raised concern because HDACs are required for brain function. We have previously shown that a triple combination formulation (TCF) of the pan HDACi vorinostat (Vo), 2-hydroxypropyl-beta-cyclodextrin (HPBCD) and polyethylene glycol (PEG) 400 improves pharmacokinetic exposure and entry of Vo into the brain. TCF treatment significantly delayed both neurodegeneration and death in the Npc1 murine model of Niemann-Pick Type C (NPC) disease. The TCF induces no metabolic toxicity, but its risk to normal brain functions and potential utility in treating lung disease, a major NPC clinical complication, remain unknown. Here we report that TCF administered in healthy mice for 8-10 months was not detrimental to the brain or neuromuscular functions based on quantitative analyses of Purkinje neurons, neuroinflammation, neurocognitive/muscular disease symptom progression, cerebellar/hippocampal nerve fiber-staining, and Hdac gene-expression. The TCF also improved delivery of Vo to lungs and reduced accumulation of foamy macrophages in Npc1 mice, with no injury. Together, these data support feasibility of tolerable, chronic administration of an HDACi formulation that treats murine NPC neurological disease and lung pathology, a frequent cause of death in this and possibly additional disorders.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:In-Data-Review
[do] DOI:10.1038/s41598-018-22162-7

  3 / 2401 MEDLINE  
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[PMID]: 29496136
[Au] Autor:Alafuzoff I
[Ad] Address:Department of Immunology, Genetics and Pathology, Uppsala University; Department of Clinical and Surgical Pathology, Uppsala University Hospital and Rudbeck Laboratory, Uppsala, Sweden. Electronic address: irina.alafuzoff@igp.uu.se.
[Ti] Title:Minimal neuropathologic diagnosis for brain banking in the normal middle-aged and aged brain and in neurodegenerative disorders.
[So] Source:Handb Clin Neurol;150:131-141, 2018.
[Is] ISSN:0072-9752
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Research on human brain diseases is currently often conducted on cell cultures and animals. Several questions however can only be addressed by studying human postmortem brain tissue. However, brain tissue obtained postmortem almost always displays pathology that is often related to the aging phenomenon. Thus, in order to be certain that the answers obtained are reliable, a systematic and thorough assessment of the brain tissue to be studied should be carried out. We are currently aware of several protein alterations that are found in middle-aged and aged brains that are obtained from neurologically unimpaired subjects. The most common alteration is hyperphosphorylation of τ, observed in both neurons and glial cells, in certain brain regions, followed by ß-amyloid aggregation in the neuropil and vessel walls. Less common protein alterations are those noted for α-synuclein and Tar DNA-binding protein 43. It is noteworthy that these alterations, when found in excess, are diagnostic for various neurodegenerative diseases, such as Alzheimer disease, Pick disease, progressive supranuclear palsy, corticobasal degeneration, Parkinson disease, Lewy body dementia, and frontotemporal lobar degeneration. Since 1990, the neuropathology community has been aware that these protein alterations tend to progress in an orderly neuroanatomically defined manner and have thus designed a method to define a stage or a phase of the protein alteration. The neuropathology community has defined an initiation site, or neuroanatomic area that they presume the alteration originates from, and defined a presumed pattern of progression from the initiation site to other brain areas. Thus a reliable and reproducible description of each case regarding these alterations can be achieved. In addition to the above alterations, the brain tissue is also prone to various vascular alterations that should be registered as seen or not seen even if the significance of these alterations is still unclear.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180302
[Lr] Last revision date:180302
[St] Status:In-Process

  4 / 2401 MEDLINE  
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[PMID]: 29309493
[Au] Autor:Santos-Santos MA; Rabinovici GD; Iaccarino L; Ayakta N; Tammewar G; Lobach I; Henry ML; Hubbard I; Mandelli ML; Spinelli E; Miller ZA; Pressman PS; O'Neil JP; Ghosh P; Lazaris A; Meyer M; Watson C; Yoon SJ; Rosen HJ; Grinberg L; Seeley WW; Miller BL; Jagust WJ; Gorno-Tempini ML
[Ad] Address:Department of Neurology, Memory and Aging Center, University of California San Francisco.
[Ti] Title:Rates of Amyloid Imaging Positivity in Patients With Primary Progressive Aphasia.
[So] Source:JAMA Neurol;, 2018 Jan 08.
[Is] ISSN:2168-6157
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Importance: The ability to predict the pathology underlying different neurodegenerative syndromes is of critical importance owing to the advent of molecule-specific therapies. Objective: To determine the rates of positron emission tomography (PET) amyloid positivity in the main clinical variants of primary progressive aphasia (PPA). Design, Setting, and Participants: This prospective clinical-pathologic case series was conducted at a tertiary research clinic specialized in cognitive disorders. Patients were evaluated as part of a prospective, longitudinal research study between January 2002 and December 2015. Inclusion criteria included clinical diagnosis of PPA; availability of complete speech, language, and cognitive testing; magnetic resonance imaging performed within 6 months of the cognitive evaluation; and PET carbon 11-labeled Pittsburgh Compound-B or florbetapir F 18 brain scan results. Of 109 patients referred for evaluation of language symptoms who underwent amyloid brain imaging, 3 were excluded because of incomplete language evaluations, 5 for absence of significant aphasia, and 12 for presenting with significant initial symptoms outside of the language domain, leaving a cohort of 89 patients with PPA. Main Outcomes and Measures: Clinical, cognitive, neuroimaging, and pathology results. Results: Twenty-eight cases were classified as imaging-supported semantic variant PPA (11 women [39.3%]; mean [SD] age, 64 [7] years), 31 nonfluent/agrammatic variant PPA (22 women [71.0%]; mean [SD] age, 68 [7] years), 26 logopenic variant PPA (17 women [65.4%]; mean [SD] age, 63 [8] years), and 4 mixed PPA cases. Twenty-four of 28 patients with semantic variant PPA (86%) and 28 of 31 patients with nonfluent/agrammatic variant PPA (90%) had negative amyloid PET scan results, while 25 of 26 patients with logopenic variant PPA (96%) and 3 of 4 mixed PPA cases (75%) had positive scan results. The amyloid positive semantic variant PPA and nonfluent/agrammatic variant PPA cases with available autopsy data (2 of 4 and 2 of 3, respectively) all had a primary frontotemporal lobar degeneration and secondary Alzheimer disease pathologic diagnoses, whereas autopsy of 2 patients with amyloid PET-positive logopenic variant PPA confirmed Alzheimer disease. One mixed PPA patient with a negative amyloid PET scan had Pick disease at autopsy. Conclusions and Relevance: Primary progressive aphasia variant diagnosis according to the current classification scheme is associated with Alzheimer disease biomarker status, with the logopenic variant being associated with carbon 11-labeled Pittsburgh Compound-B positivity in more than 95% of cases. Furthermore, in the presence of a clinical syndrome highly predictive of frontotemporal lobar degeneration pathology, biomarker positivity for Alzheimer disease may be associated more with mixed pathology rather than primary Alzheimer disease.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180302
[Lr] Last revision date:180302
[St] Status:Publisher
[do] DOI:10.1001/jamaneurol.2017.4309

  5 / 2401 MEDLINE  
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[PMID]: 29377514
[Au] Autor:Akilo OD; Kumar P; Choonara YE; Pradeep P; du Toit LC; Pillay V
[Ad] Address:Wits Advanced Drug Delivery Platform Research Unit, Department of Pharmacy and Pharmacology, School of Therapeutic Sciences, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa.
[Ti] Title:Hypothesis: apo-lactoferrin-Galantamine Proteo-alkaloid Conjugate for Alzheimer's disease Intervention.
[So] Source:J Cell Mol Med;22(3):1957-1963, 2018 Mar.
[Is] ISSN:1582-4934
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Alzheimer's disease (AD) is known to be caused by the accumulation of deformed beta amyloid and hyperphosphorylated tau proteins resulting into formation and aggregation of senile plaques and neurofibrillary tangles in the brain. Additionally, AD is associated with the accumulation of iron or metal ions in the brain which causes oxidative stress. Galantamine (Gal) is one of the therapeutic agents that has been approved for the treatment of AD, but still saddled with numerous side effects and could not address the issue of iron accumulation in the brain. The use of metal chelators to address the iron accumulation has not been successful due to toxicity and inability to address the aggregation of the plaques. We therefore hypothesize a combinatorial antioxidant-metal-chelator approach by formulating a single dosage form that has the ability to prevent the formation of free radicals, plaques and accumulation of iron in the brain. This can be achieved by conjugating Gal with apo-lactoferrin (ApoLf), a natural compound that has high binding affinity for iron, to form an apo-lactoferrin-galantamine proteo-alkaloid conjugate (ApoLf-Gal) as a single dosage form for AD management. The conjugation is achieved through self-assembly of ApoLf which results in encapsulation of Gal. ApoLf changes its conformational structure in the presence of iron; therefore, ApoLf-Gal is proposed to deliver Gal and pick up excess iron when in contact with iron. This strategy has the potential to proffer a dual neuroprotection and neurotherapeutic interventions for the management of AD.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180301
[Lr] Last revision date:180301
[St] Status:In-Data-Review
[do] DOI:10.1111/jcmm.13484

  6 / 2401 MEDLINE  
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[PMID]: 29476982
[Au] Autor:Dill V; Klein PC; Franco AR; Pinho MS
[Ad] Address:School of Technology, PUCRS, Porto Alegre, Brazil.
[Ti] Title:Atlas selection for hippocampus segmentation: Relevance evaluation of three meta-information parameters.
[So] Source:Comput Biol Med;95:90-98, 2018 Feb 09.
[Is] ISSN:1879-0534
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Current state-of-the-art methods for whole and subfield hippocampus segmentation use pre-segmented templates, also known as atlases, in the pre-processing stages. Typically, the input image is registered to the template, which provides prior information for the segmentation process. Using a single standard atlas increases the difficulty in dealing with individuals who have a brain anatomy that is morphologically different from the atlas, especially in older brains. To increase the segmentation precision in these cases, without any manual intervention, multiple atlases can be used. However, registration to many templates leads to a high computational cost. Researchers have proposed to use an atlas pre-selection technique based on meta-information followed by the selection of an atlas based on image similarity. Unfortunately, this method also presents a high computational cost due to the image-similarity process. Thus, it is desirable to pre-select a smaller number of atlases as long as this does not impact on the segmentation quality. To pick out an atlas that provides the best registration, we evaluate the use of three meta-information parameters (medical condition, age range, and gender) to choose the atlas. In this work, 24 atlases were defined and each is based on the combination of the three meta-information parameters. These atlases were used to segment 352 vol from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database. Hippocampus segmentation with each of these atlases was evaluated and compared to reference segmentations of the hippocampus, which are available from ADNI. The use of atlas selection by meta-information led to a significant gain in the Dice similarity coefficient, which reached 0.68 ±â€¯0.11, compared to 0.62 ±â€¯0.12 when using only the standard MNI152 atlas. Statistical analysis showed that the three meta-information parameters provided a significant improvement in the segmentation accuracy.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180224
[Lr] Last revision date:180224
[St] Status:Publisher

  7 / 2401 MEDLINE  
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[PMID]: 29397865
[Au] Autor:Park MH; Lee JY; Jeong MS; Jang HS; Endo S; Bae JS; Jin HK
[Ad] Address:Stem Cell Neuroplasticity Research Group, Kyungpook National University, Daegu 41566; Department of Physiology, Cell and Matrix Research Institute, School of Medicine, Kyungpook National University, Daegu 41944; Department of Biomedical Science, BK21 Plus KNU Biomedical Convergence Program, Kyungpoo
[Ti] Title:The role of Purkinje cell-derived VEGF in cerebellar astrogliosis in Niemann-Pick type C mice.
[So] Source:BMB Rep;51(2):79-84, 2018 Feb.
[Is] ISSN:1976-670X
[Cp] Country of publication:Korea (South)
[La] Language:eng
[Ab] Abstract:Niemann-Pick type C disease (NP-C) is a fatal neurodegenerative disorder caused by a deficiency of NPC1 gene function, which leads to severe neuroinflammation such as astrogliosis. While reports demonstrating neuroinflammation are prevalent in NP-C, information about the onset and progression of cerebellar astrogliosis in this disorder is lacking. Using gene targeting, we generated vascular endothelial growth factor (VEGF) conditional null mutant mice. Deletion of VEGF in cerebellar Purkinje neurons (PNs) led to a significant increase of astrogliosis in the brain of NP-C mice in addition to the loss of PNs, suggesting PN-derived VEGF as an important factor in NP-C pathology. Moreover, replenishment of VEGF in neurons improved brain pathology in NP-C mice. Overall, our data provide a new pathological perspective on cerebellar astrogliosis in NP-C and suggest the importance of VEGF as a therapeutic target for this disease. [BMB Reports 2018; 51(2): 79-84].
[Pt] Publication type:NEWS
[Em] Entry month:1802
[Cu] Class update date: 180223
[Lr] Last revision date:180223
[St] Status:In-Process

  8 / 2401 MEDLINE  
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[PMID]: 29346563
[Au] Autor:Gurda BL; Bagel JH; Fisher SJ; Schultz ML; Lieberman AP; Hand P; Vite CH; Swain GP
[Ad] Address:Department of Clinical Sciences and Advanced Medicine, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
[Ti] Title:LC3 Immunostaining in the Inferior Olivary Nuclei of Cats With Niemann-Pick Disease Type C1 Is Associated With Patterned Purkinje Cell Loss.
[So] Source:J Neuropathol Exp Neurol;77(3):229-245, 2018 Mar 01.
[Is] ISSN:1554-6578
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The feline model of Niemann-Pick disease, type C1 (NPC1) recapitulates the clinical, neuropathological, and biochemical abnormalities present in children with NPC1. The hallmarks of disease are the lysosomal storage of unesterified cholesterol and multiple sphingolipids in neurons, and the spatial and temporal distribution of Purkinje cell death. In feline NPC1 brain, microtubule-associated protein 1 light chain 3 (LC3) accumulations, indicating autophagosomes, were found within axons and presynaptic terminals. High densities of accumulated LC3 were seen in subdivisions of the inferior olive, which project to cerebellar regions that show the most Purkinje cell loss, suggesting that autophagic abnormalities in specific climbing fibers may contribute to the spatial pattern of Purkinje cell loss seen. Biweekly intrathecal administration of 2-hydroxypropyl-beta cyclodextrin (HPßCD) ameliorated neurological dysfunction, reduced cholesterol and sphingolipid accumulation, and increased lifespan in NPC1 cats. LC3 pathology was reduced in treated animals suggesting that HPßCD administration also ameliorates autophagic abnormalities. This study is the first to (i) identify specific brain regions exhibiting autophagic abnormalities in any species with NPC1, (ii) provide evidence of differential vulnerability among discrete brain nuclei and pathways, and (iii) show the amelioration of these abnormalities in NPC1 cats treated with HPßCD.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180216
[Lr] Last revision date:180216
[St] Status:In-Data-Review
[do] DOI:10.1093/jnen/nlx119

  9 / 2401 MEDLINE  
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[PMID]: 29411332
[Au] Autor:Erickson RP; Deutsch G; Patil R
[Ad] Address:Department of Pediatrics, University of Arizona College of Medicine, Tucson, AZ, USA. erickson@pediatrics.arizona.edu.
[Ti] Title:A pilot study of direct delivery of hydroxypropyl-beta-cyclodextrin to the lung by the nasal route in a mouse model of Niemann-Pick C1 disease: motor performance is unaltered and lung disease is worsened.
[So] Source:J Appl Genet;, 2018 Feb 06.
[Is] ISSN:2190-3883
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:We have tested the efficacy of hydroxypropyl-beta-cyclodextrin (HPBCD) delivered by the nasal route in the mouse model of juvenile Niemann-Pick C1 disease (NPC1), as pulmonary disease has not responded to systemic therapy with this drug. Since mice have no gag reflex, coating of the nasal cavity, with possible access to the brain, would be followed by delivery of HPBCD to the lung. While foamy macrophages, containing stored cholesterol, were found in the Npc1 homozygous mice, a marked inflammatory response was found with inhaled HPBCD, both in mutant and wild-type animals. Slight inflammation also occasionally occurred with saline inhalation. There was no difference between the saline-treated, HPBCD-treated, and untreated Npc1 homozygous mice for weight, balance beam performance, or coat hanger performance. Interestingly, there was a trend to longer survival in the HPBCD-treated Npc1 homozygous mice, which, when combined with the survival times of the saline-treated survivals (each of which was not different), became significant.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180207
[Lr] Last revision date:180207
[St] Status:Publisher
[do] DOI:10.1007/s13353-018-0431-z

  10 / 2401 MEDLINE  
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[PMID]: 29397615
[Au] Autor:Ren SC; Tian ZX; Deng YX; Wang YJ; Wu XJ; Zhang YZ; Gao BQ
[Ad] Address:Department of Pediatric, Beijing Tian Tan Hospital, Capital Medical University, Beijing 100050, China.
[Ti] Title:[Clinical features and gene mutation analysis of patients with Niemann-Pick disease type C].
[So] Source:Zhonghua Yi Xue Za Zhi;98(4):284-288, 2018 Jan 23.
[Is] ISSN:0376-2491
[Cp] Country of publication:China
[La] Language:chi
[Ab] Abstract:To analyze the clinical manifestations, therapeutic efficacy, prognosis and characteristics of NPC1 mutation in Chinese patients with Niemann-Pick disease type C(NPC). Ten unrelated Chinese NPC patients were diagnosed by NPC1 mutation analysis from July 2013 to February 2017 in Beijing Tian Tan Hospital of Capital Medical University. Clinical data of 10 cases were analyzed retrospectively which included clinical manifestations, laboratory results and NPC1 gene mutation features, and a series of follow-up were carried out about therapeutic efficacy and prognosis. Ten patients suffering from NPC included 5 males and 5 females, aged from 42 days to 14 years when they presented to Tian Tan Hospital. According to their age of neurological onset, 4 were in early infantile period, 2 in late infantile period, 2 in juvenile periods, and the other 2 cases in neonatal period. They all presented with splenomegaly, 5 of 10 accompanied with hepatomegaly. Two cases of neonatal subtype presented mainly with delayed neonatal cholestatic jaundice and hepatosplenomegaly, accompanied with decreased muscle tone and slight psychomotor retardation. The other 8 cases presented with severe neurological involvement, such as progressive encephalopathy, ataxia and language impairment, 4 with dystonia, 3 with decreased muscle tension, 5 with vertical supranuclear gaze palsy, 5 with gelastic cataplexy, and 4 with epilepsy. Eight of 9 cases presented with foam cells in their bone marrow. Head MRI showed diffuse cerebral atrophy in 8 cases, thin corpus callosum in 2 cases, and brain white matter abnormal signals in 2 cases. Among 10 cases, 18 different mutations of NPC1 allelic genes were identified including 11 reported mutations, 3 novel missense mutations: c. 3683T>C (p.Met1128Thr), c.1926G>C (p.Met642Iie) and c. 3006C>G (p.Phe1002Leu), 2 novel nonsense mutation: c. 1142G>A(p.Trp381Ter ) and c. 3229C>T(p.Arg1077Ter), 1 novel minimal deletion mutation: c. 1385-1386del, and 1 novel intron mutation: c. 1757+ 5G>A. In 5 cases, the symptom of gelastic cataplexy was alleviated by imipramine, and the convulsion was relieved by valproate in 2 cases, by carbamazepine in 1 case at the beginning of seizure. During the 25 (3-66) months of follow-up, 4 cases died, the others' neurological symptoms were deteriorated progressively. The NPC1 gene mutation were high heterozygous in this group, and 7 novel mutations enriched the gene mutation spectrum of NPC1. The neurological manifestations were complicated in patients with NPC, and the symptomatology would be different according to their onset age of neurological symptoms. There might be effective symptomatic treatment for gelastic cataplexy by imipramine and for convulsion by valproate or carbamazepine.
[Pt] Publication type:ENGLISH ABSTRACT; JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180205
[Lr] Last revision date:180205
[St] Status:In-Process
[do] DOI:10.3760/cma.j.issn.0376-2491.2018.04.009


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