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[PMID]: 25876686
[Au] Autor:Sun L; Kuang X; Hao S; Wang P; Niu X; Zhu G; Zhou J; Huang W
[Ad] Address:Department of Nephrology and Rheumatology, Children's Hospital of Shanghai Jiao Tong University, Shanghai 200062, China.
[Ti] Title:[Features of clinical phenotype and genotype in Alport syndrome: a monocentric study].
[So] Source:Zhonghua Er Ke Za Zhi;53(2):114-8, 2015 Feb.
[Is] ISSN:0578-1310
[Cp] Country of publication:China
[La] Language:chi
[Ab] Abstract:OBJECTIVE: To analyze the clinical features and gene mutation of Chinese children with Alport syndrome(AS). METHOD: From May 2011 to May 2014, clinical and pathological information gathered from 25 patients was retrospectively analyzed. COL4A5, COL4A4 and COL4A3 genes were analyzed using next-generation sequencing in these patients, and gene mutations of related family members were identified by Sanger method. RESULT: Of these 25 cases, 19(76%) had X-linked Alport syndromes (XL-AS), 6 had autosomal recessive Alport syndromes (AR-AS). Twenty five patients had an onset of hematuria and proteinuria and in 8 cases the disease was induced by upper respiratory tract infections. Hearing loss was present in 2 of 25 (8%) cases and ocular lesions in 1 of 25 (4%). Renal pathology showed that 16 of them had minimal change disease (MCD), 8 mesangial proliferative glomerulonephritis (MsPNG), 1 focal segmental glomerulo-sclerosis (FSGS). Extensive lamination and split of glomerular basement membrane (GBM) dense layers were found in 2 (8%) of 25 patients. Twenty one of 25 patients (84%) showed abnormal renal α-chain distribution. COL4A5, COL4A4 and COL4A3 genes of 25 patients (23 families) were analyzed and 24 pathogenic mutations were identified: 18 in COL4A5, 1 in COL4A3 and 5 in COL4A4. It was observed that 13 patients inherited the mutation from the mother, 3 patients inherited from the father, 2 patients inherited 1 mutation from the mother and another mutation from the father, and 7 patients carried the novel mutations. CONCLUSION: XL is the main inherited type in AS. Most of patients showed MCD and MsPNG in renal biopsy. This research examined 24 mutations and 16 mutations were not reported previously.
[Mh] MeSH terms primary: Mutation
Nephritis, Hereditary/genetics
Nephritis, Hereditary/pathology
[Mh] MeSH terms secundary: Child
Deafness
Genes, Recessive
Genotype
Hematuria
Humans
Kidney
Pedigree
Phenotype
[Pt] Publication type:ENGLISH ABSTRACT; JOURNAL ARTICLE
[Em] Entry month:1505
[Js] Journal subset:IM
[Da] Date of entry for processing:150416
[St] Status:MEDLINE

  2 / 185393 MEDLINE  
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[PMID]: 25840091
[Au] Autor:Haddad RN; Mielniczuk LM
[Ad] Address:Department of Cardiology, University of Ottawa Heart Institute, Ottawa, Ontario, Canada.
[Ti] Title:An evidence-based approach to screening and diagnosis of pulmonary hypertension.
[So] Source:Can J Cardiol;31(4):382-90, 2015 Apr.
[Is] ISSN:1916-7075
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Pulmonary hypertension (PH) continues to be a devastating disease, with a poor prognosis and high mortality rate if not treated early. Unfortunately, most patients are still diagnosed late in the course of the disease. Therefore, it is crucial to have a low threshold for suspecting PH and to refer patients early to specialized centres for diagnostic workup and management. In this article we focus on updated evidence-based screening and diagnosis in adults, based on the fifth World Symposium on Pulmonary Hypertension in 2013. The updated hemodynamic definition of PH includes a pulmonary vascular resistance > 3 Wood units. A new component to the hemodynamic definition of PH has been proposed in left heart disease, based on a diastolic pulmonary gradient (diastolic pulmonary arterial pressure - mean pulmonary artery wedge pressure), > 7 mm Hg. The term "borderline PH" for mean pulmonary artery pressures 21-24 mm Hg is discouraged, with emphasis on its significance for careful follow-up in high-risk patients, especially in systemic sclerosis. Annual pulmonary arterial hypertension (PAH) screening with a 2-step algorithm is recommended in asymptomatic systemic sclerosis patients. An updated simplified PH diagnostic algorithm approach is proposed. Genetic testing reveals mutations in bone morphogenic protein receptor type II in 70% of familial PAH, and is useful for screening asymptomatic family members. Important associated conditions that should be considered include thyroid disease, left heart disease, toxic causes, lung diseases (including pulmonary thromboembolism), hemolytic anemia, and human immunodeficiency virus infection. Biomarkers have been identified that correlate with PAH severity and mortality and are useful in follow-up.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Em] Entry month:1504
[Js] Journal subset:IM
[St] Status:In-Data-Review

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[PMID]: 25316630
[Au] Autor:Marangi G; Traynor BJ
[Ad] Address:Neuromuscular Diseases Research Section, Laboratory of Neurogenetics, National Institute on Aging, Bethesda, MD, USA; Institute of Medical Genetics, Catholic University, Roma, Italy. Electronic address: giuseppe.marangi@rm.unicatt.it.
[Ti] Title:Genetic causes of amyotrophic lateral sclerosis: new genetic analysis methodologies entailing new opportunities and challenges.
[So] Source:Brain Res;1607:75-93, 2015 May 14.
[Is] ISSN:1872-6240
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:The genetic architecture of amyotrophic lateral sclerosis (ALS) is being increasingly understood. In this far-reaching review, we examine what is currently known about ALS genetics and how these genes were initially identified. We also discuss the various types of mutations that might underlie this fatal neurodegenerative condition and outline some of the strategies that might be useful in untangling them. These include expansions of short repeat sequences, common and low-frequency genetic variations, de novo mutations, epigenetic changes, somatic mutations, epistasis, oligogenic and polygenic hypotheses. This article is part of a Special Issue entitled ALS complex pathogenesis.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1504
[Js] Journal subset:IM
[St] Status:In-Data-Review

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[PMID]: 25289585
[Au] Autor:Casci I; Pandey UB
[Ad] Address:Department of Pediatrics, Child Neurology and Neurobiology, Children׳s Hospital of Pittsburgh, University of Pittsburgh Medical Center, Pittsburgh, PA 15224, USA; Human Genetics Graduate Program, University of Pittsburgh School of Public Health, Pittsburgh, PA 15261, USA.
[Ti] Title:A fruitful endeavor: modeling ALS in the fruit fly.
[So] Source:Brain Res;1607:47-74, 2015 May 14.
[Is] ISSN:1872-6240
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:For over a century Drosophila melanogaster, commonly known as the fruit fly, has been instrumental in genetics research and disease modeling. In more recent years, it has been a powerful tool for modeling and studying neurodegenerative diseases, including the devastating and fatal amyotrophic lateral sclerosis (ALS). The success of this model organism in ALS research comes from the availability of tools to manipulate gene/protein expression in a number of desired cell-types, and the subsequent recapitulation of cellular and molecular phenotypic features of the disease. Several Drosophila models have now been developed for studying the roles of ALS-associated genes in disease pathogenesis that allowed us to understand the molecular pathways that lead to motor neuron degeneration in ALS patients. Our primary goal in this review is to highlight the lessons we have learned using Drosophila models pertaining to ALS research. This article is part of a Special Issue entitled ALS complex pathogenesis.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Em] Entry month:1504
[Js] Journal subset:IM
[St] Status:In-Data-Review

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[PMID]: 25261695
[Au] Autor:Mendez EF; Sattler R
[Ad] Address:Brain Science Institute and Department of Neurology, Johns Hopkins University School of Medicine, 855N Wolfe Street, Rangos 2-223, Baltimore, MD 21205, USA.
[Ti] Title:Biomarker development for C9orf72 repeat expansion in ALS.
[So] Source:Brain Res;1607:26-35, 2015 May 14.
[Is] ISSN:1872-6240
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:The expanded GGGGCC hexanucleotide repeat in the non-coding region of the C9orf72 gene on chromosome 9p21 has been discovered as the cause of approximately 20-50% of familial and up to 5-20% of sporadic amyotrophic lateral sclerosis (ALS) cases, making this the most common known genetic mutation of ALS to date. At the same time, it represents the most common genetic mutation in frontotemporal dementia (FTD; 10-30%). Because of the high prevalence of mutant C9orf72, pre-clinical efforts in identifying therapeutic targets and developing novel therapeutics for this mutation are highly pursued in the hope of providing a desperately needed disease-modifying treatment for ALS patients, as well as other patient populations affected by the C9orf72 mutation. The current lack of effective treatments for ALS is partially due to the lack of appropriate biomarkers that aide in assessing drug efficacy during clinical trials independent of clinical outcome measures, such as increased survival. In this review we will summarize the opportunities for biomarker development specifically targeted to the newly discovered C9orf72 repeat expansion. While drugs are being developed for this mutation, it will be crucial to provide a reliable biomarker to accompany the clinical development of these novel therapeutic interventions to maximize the chances of a successful clinical trial. This article is part of a Special Issue entitled ALS complex pathogenesis.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Em] Entry month:1504
[Js] Journal subset:IM
[St] Status:In-Data-Review

  6 / 185393 MEDLINE  
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[PMID]: 25223906
[Au] Autor:Richard JP; Maragakis NJ
[Ad] Address:Johns Hopkins University, School of Medicine, USA.
[Ti] Title:Induced pluripotent stem cells from ALS patients for disease modeling.
[So] Source:Brain Res;1607:15-25, 2015 May 14.
[Is] ISSN:1872-6240
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:The ability to reprogram adult somatic cells into pluripotent stem cells that can differentiate into all three germ layers of the developing human has fundamentally changed the landscape of biomedical research. For a neurodegenerative disease like Amyotrophic Lateral Sclerosis (ALS), which does not manifest itself until adulthood and is a heterogeneous disease with few animal models, this technology may be particularly important. Induced pluripotent stem cells (iPSC) have been created from patients with several familial forms of ALS as well as some sporadic forms of ALS. These cells have been differentiated into ALS-relevant cell subtypes including motor neurons and astrocytes, among others. ALS-relevant pathologies have also been identified in motor neurons from these cells and may provide a window into understanding disease mechanisms in vitro. Given that this is a relatively new field of research, numerous challenges remain before iPSC methodologies can fulfill their potential as tools for modeling ALS as well as providing a platform for the investigation of ALS therapeutics. This article is part of a Special Issue entitled ALS complex pathogenesis.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.; REVIEW
[Em] Entry month:1504
[Js] Journal subset:IM
[St] Status:In-Data-Review

  7 / 185393 MEDLINE  
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[PMID]: 25175835
[Au] Autor:Jablonski M; Miller DS; Pasinelli P; Trotti D
[Ad] Address:Weinberg Unit for ALS Research, Farber Institute for Neurosciences, Department of Neuroscience, Thomas Jefferson University, 900 Walnut Street, Philadelphia, PA 19004, USA. Electronic address: Michael.jablonski@jefferson.edu....
[Ti] Title:ABC transporter-driven pharmacoresistance in Amyotrophic Lateral Sclerosis.
[So] Source:Brain Res;1607:1-14, 2015 May 14.
[Is] ISSN:1872-6240
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Amyotrophic Lateral Sclerosis (ALS) is a slowly progressing neurodegenerative disease that affects motor neurons of the nervous system. Despite the identification of many potential therapeutics targeting pathogenic mechanisms in in vitro models, there has been limited progress in translating them into a successful pharmacotherapy in the animal model of ALS. Further, efforts to translate any promising results from preclinical trials to effective pharmacotherapies for patients have been unsuccessful, with the exception of riluzole, the only FDA-approved medication, which only modestly extends survival both in the animal model and in patients. Thus, it is essential to reconsider the strategies for developing ALS pharmacotherapies. Growing evidence suggests that problems identifying highly effective ALS treatments may result from an underestimated issue of drug bioavailability and disease-driven pharmacoresistance, mediated by the ATP-binding cassette (ABC) drug efflux transporters. ABC transporters are predominately localized to the lumen of endothelial cells of the blood-brain and blood-spinal cord barriers (BBB, BSCB) where they limit the entry into the central nervous system (CNS) of a wide range of neurotoxicants and xenobiotics, but also therapeutics. In ALS, expression and function of ABC transporters is increased at the BBB/BSCB and their expression has been detected on neurons and glia in the CNS parenchyma, which may further reduce therapeutic action in target cells. Understanding and accounting for the contribution of these transporters to ALS pharmacoresistance could both improve the modest effects of riluzole and set in motion a re-evaluation of previous ALS drug disappointments. In addition, identifying pathogenic mechanisms regulating ABC transporter expression and function in ALS may lead to the development of new therapeutic strategies. It is likely that novel pharmacological approaches require counteracting pharmacoresistance to improve therapeutic efficacy. This article is part of a Special Issue entitled ALS complex pathogenesis.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, N.I.H., INTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.; REVIEW
[Em] Entry month:1504
[Js] Journal subset:IM
[St] Status:In-Data-Review

  8 / 185393 MEDLINE  
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[PMID]: 25700176
[Au] Autor:Cirulli ET; Lasseigne BN; Petrovski S; Sapp PC; Dion PA; Leblond CS; Couthouis J; Lu YF; Wang Q; Krueger BJ; Ren Z; Keebler J; Han Y; Levy SE; Boone BE; Wimbish JR; Waite LL; Jones AL; Carulli JP; Day-Williams AG; Staropoli JF; Xin WW; Chesi A; Raphael AR; McKenna-Yasek D; Cady J; Vianney de Jong JM; Kenna KP; Smith BN; Topp S; Miller J; Gkazi A; Al-Chalabi A; van den Berg LH; Veldink J; Silani V; Ticozzi N; Shaw CE; Baloh RH; Appel S; Simpson E; Lagier-Tourenne C; Pulst SM; Gibson S; Trojanowski JQ; Elman L; McCluskey L; Grossman M; Shneider NA; Chung WK; FALS Sequencing Consortium
[Ad] Address:Center for Applied Genomics and Precision Medicine, Duke University School of Medicine, Durham, NC 27708, USA....
[Ti] Title:Exome sequencing in amyotrophic lateral sclerosis identifies risk genes and pathways.
[So] Source:Science;347(6229):1436-41, 2015 Mar 27.
[Is] ISSN:1095-9203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Amyotrophic lateral sclerosis (ALS) is a devastating neurological disease with no effective treatment. We report the results of a moderate-scale sequencing study aimed at increasing the number of genes known to contribute to predisposition for ALS. We performed whole-exome sequencing of 2869 ALS patients and 6405 controls. Several known ALS genes were found to be associated, and TBK1 (the gene encoding TANK-binding kinase 1) was identified as an ALS gene. TBK1 is known to bind to and phosphorylate a number of proteins involved in innate immunity and autophagy, including optineurin (OPTN) and p62 (SQSTM1/sequestosome), both of which have also been implicated in ALS. These observations reveal a key role of the autophagic pathway in ALS and suggest specific targets for therapeutic intervention.
[Mh] MeSH terms primary: Amyotrophic Lateral Sclerosis/genetics
Autophagy/genetics
Exome/genetics
Genetic Predisposition to Disease
Protein-Serine-Threonine Kinases/genetics
[Mh] MeSH terms secundary: Adaptor Proteins, Signal Transducing/genetics
Adaptor Proteins, Signal Transducing/metabolism
Adolescent
Adult
Aged
Aged, 80 and over
Female
Genes
Genetic Association Studies
Humans
Male
Middle Aged
Protein Binding
Protein-Serine-Threonine Kinases/metabolism
Risk
Sequence Analysis, DNA
Transcription Factor TFIIIA/genetics
Transcription Factor TFIIIA/metabolism
Young Adult
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Adaptor Proteins, Signal Transducing); 0 (OPTN protein, human); 0 (SQSTM1 protein, human); 0 (Transcription Factor TFIIIA); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (TBK1 protein, human)
[Em] Entry month:1504
[Cu] Class update date: 150516
[Lr] Last revision date:150516
[Js] Journal subset:IM
[Da] Date of entry for processing:150327
[St] Status:MEDLINE
[do] DOI:10.1126/science.aaa3650

  9 / 185393 MEDLINE  
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[PMID]: 25671101
[Au] Autor:Anderson KM; Olson KE; Estes KA; Flanagan K; Gendelman HE; Mosley RL
[Ad] Address:Department of Pharmacology and Experimental Neuroscience, Center for Neurodegenerative Disorders, The University of Nebraska Medical Center, Omaha, NE 68198 USA....
[Ti] Title:Dual destructive and protective roles of adaptive immunity in neurodegenerative disorders.
[So] Source:Transl Neurodegener;3(1):25, 2014.
[Is] ISSN:2047-9158
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Inappropriate T cell responses in the central nervous system (CNS) affect the pathogenesis of a broad range of neuroinflammatory and neurodegenerative disorders that include, but are not limited to, multiple sclerosis, amyotrophic lateral sclerosis, Alzheimer's disease and Parkinson's disease. On the one hand immune responses can exacerbate neurotoxic responses; while on the other hand, they can lead to neuroprotective outcomes. The temporal and spatial mechanisms by which these immune responses occur and are regulated in the setting of active disease have gained significant recent attention. Spatially, immune responses that affect neurodegeneration may occur within or outside the CNS. Migration of antigen-specific CD4+ T cells from the periphery to the CNS and consequent immune cell interactions with resident glial cells affect neuroinflammation and neuronal survival. The destructive or protective mechanisms of these interactions are linked to the relative numerical and functional dominance of effector or regulatory T cells. Temporally, immune responses at disease onset or during progression may exhibit a differential balance of immune responses in the periphery and within the CNS. Immune responses with predominate T cell subtypes may differentially manifest migratory, regulatory and effector functions when triggered by endogenous misfolded and aggregated proteins and cell-specific stimuli. The final result is altered glial and neuronal behaviors that influence the disease course. Thus, discovery of neurodestructive and neuroprotective immune mechanisms will permit potential new therapeutic pathways that affect neuronal survival and slow disease progression.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1502
[Cu] Class update date: 150516
[Lr] Last revision date:150516
[Da] Date of entry for processing:150211
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.1186/2047-9158-3-25

  10 / 185393 MEDLINE  
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[PMID]: 25433341
[Au] Autor:Sea K; Sohn SH; Durazo A; Sheng Y; Shaw BF; Cao X; Taylor AB; Whitson LJ; Holloway SP; Hart PJ; Cabelli DE; Gralla EB; Valentine JS
[Ad] Address:From the Department of Chemistry and Biochemistry, University of California, Los Angeles, California 90095, the Department of Wine Studies, Santa Rosa Junior College, Santa Rosa, California 95401, kevinsea@yahoo.com....
[Ti] Title:Insights into the role of the unusual disulfide bond in copper-zinc superoxide dismutase.
[So] Source:J Biol Chem;290(4):2405-18, 2015 Jan 23.
[Is] ISSN:1083-351X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The functional and structural significance of the intrasubunit disulfide bond in copper-zinc superoxide dismutase (SOD1) was studied by characterizing mutant forms of human SOD1 (hSOD) and yeast SOD1 lacking the disulfide bond. We determined x-ray crystal structures of metal-bound and metal-deficient hC57S SOD1. C57S hSOD1 isolated from yeast contained four zinc ions per protein dimer and was structurally very similar to wild type. The addition of copper to this four-zinc protein gave properly reconstituted 2Cu,2Zn C57S hSOD, and its spectroscopic properties indicated that the coordination geometry of the copper was remarkably similar to that of holo wild type hSOD1. In contrast, the addition of copper and zinc ions to apo C57S human SOD1 failed to give proper reconstitution. Using pulse radiolysis, we determined SOD activities of yeast and human SOD1s lacking disulfide bonds and found that they were enzymatically active at ∼10% of the wild type rate. These results are contrary to earlier reports that the intrasubunit disulfide bonds in SOD1 are essential for SOD activity. Kinetic studies revealed further that the yeast mutant SOD1 had less ionic attraction for superoxide, possibly explaining the lower rates. Saccharomyces cerevisiae cells lacking the sod1 gene do not grow aerobically in the absence of lysine, but expression of C57S SOD1 increased growth to 30-50% of the growth of cells expressing wild type SOD1, supporting that C57S SOD1 retained a significant amount of activity.
[Mh] MeSH terms primary: Mutant Proteins/chemistry
Saccharomyces cerevisiae Proteins/chemistry
Superoxide Dismutase/chemistry
[Mh] MeSH terms secundary: Amyotrophic Lateral Sclerosis/genetics
Apoproteins/chemistry
Calorimetry, Differential Scanning
Disulfides/chemistry
Electron Spin Resonance Spectroscopy
Humans
Mass Spectrometry
Metals/chemistry
Mutation
Oxidative Stress
Protein Binding
Protein Conformation
Saccharomyces cerevisiae/chemistry
Spectrometry, Mass, Electrospray Ionization
Spectrophotometry
Superoxides/chemistry
Zinc/chemistry
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Name of substance:0 (Apoproteins); 0 (Disulfides); 0 (Metals); 0 (Mutant Proteins); 0 (Saccharomyces cerevisiae Proteins); 11062-77-4 (Superoxides); EC 1.15.1.1 (Superoxide Dismutase); J41CSQ7QDS (Zinc)
[Em] Entry month:1504
[Cu] Class update date: 150516
[Lr] Last revision date:150516
[Js] Journal subset:IM
[Da] Date of entry for processing:150127
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M114.588798


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