107 Matching Annotations
  1. Last 7 days
    1. Patient 1

      Case:Patient 1, Male, 4 y/o, German and Thai

      DiseaseAssertion:FOXG1 syndrome

      FamilyInfo: Non-consanguineous parents. De novo. Patient 1 has maternally inherited duplications at 15q21.12(47292250-47309868)x3 and Xp22.31(6451676-8115124)x3 of unknown clinical significance.

      ParentalGenotype:Not provided

      CasePresentingHPOs:HP:0002197, HP:0005484, HP:0011344, HP:0001252, HP:0020045,HP:0000540, HP:0010808, HP:0002019, HP:0003781, HP:0012741, HP:0002421, HP:0000748, HP:0003763, HP:5200017, HP:0025112, HP:0000957

      CaseHPOFreeText: At 19 months, could not sit independently and no speech development. Stereotypic hand and head movements. High pain tolerance. X-ray at age 2 showed broad ribs. Improved head control by age 4.

      CaseNotHPO:HP:0410263, HP:0002376

      CaseNotHPOFreeText:Dysmorphic features. breathing abnormalities

      CasePreviousTesting:No previous testing

      PreviouslyPublished:Not previously published

      GenotypingMethod:Mate-pair sequencing, Sanger sequencing

      Gene:FOXG1

      Variant:46,XY,t(9;14)(q22.3;q11.2)dn

      HGVS:Not provided

      ClinVarID:426096

      gnomAD:Not provided

    2. Patient 3

      Case:Patient 3, Male, 1 y/o, Brazilian

      DiseaseAssertion: FOXG1 syndrome

      FamilyInfo: Non-consanguineous parents

      ParentalGenotype: No family testing mentioned.

      CasePresentingHPOs: HP:0000252, HP:0001252, HP:0000486

      CaseHPOFreeText: Developed microcephaly within 1 year. Developmental delay, unable to sit without assistance at 1 year old. Central Nervous System (CNS) MRI showed a volumetric reduction of the cerebral parenchyma, hypomyelination, and hypoplasia of corpus callosum mainly involving the anterior part and prominent lateral ventricles

      CaseNotHPO: HP:0030917

      CaseNotHPOFreeText: Normal length, weight, HC at birth. No retinal abnormalities.

      CasePreviousTesting: Not asserted.

      PreviouslyPublished: Not previously published.

      GenotypingMethod: Sanger sequencing, mate-pair sequencing

      Gene: FOXG1

      Variant: 46,XY,t(2;14)(q37;q11.2)dn

      HGVS: Not provided.

      ClinVarID:426094

      gnomAD:Not provided

    3. Patient 2

      Case:Patient 2, Female, 5 y/o, Brazilian

      DiseaseAssertion:quadriplegic cerebral palsy with axial hypotonia and distal spasticity

      FamilyInfo: Non-consanguineous parents. Parents had normal karyotypes. Older sister was clinically normal.

      ParentalGenotype: Normal karyotypes for both parents.

      CasePresentingHPOs: HP:0002098, HP:0010959, HP:0008755, HP:0002090, HP:0032661, HP:0001274, HP:0011344, HP:0001249, HP:0001344, HP:0000748, HP:0034435, HP:0000486, HP:0000483, HP:0200136

      CaseHPOFreeText: Dilated superficial blood vessels seen on brain MRI.

      CaseNotHPO:N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: Not asserted

      PreviouslyPublished: Not previously published

      GenotypingMethod:Mate-pair sequencing, Sanger sequencing, chromosome analysis

      Gene: FOXG1

      Variant: 46,XX,t(4;14)(q27;q13)dn

      HGVS: Not provided

      ClinVarID: 426095

      gnomAD: Not provided

    1. 52

      Case#:Patient 52, female, 3 years old

      DiseaseAssertion:Neonatal/Infantile Epileptic Encephalopathy (NIEE)

      FamilyInfo:DeNovo. The family is Chinese

      ParentalGenotype:The authors only conducted singleton and not trio-based exome sequencing so the parents' exomes were not sequenced.

      CasePresentingHPOs:HP:0011344, HP:0002069, HP:0007359, HP:0011097, HP:0100704, HP:0001332, HP:0002072, HP:0012171.

      CaseHPOFreeText:Patient 52 presents with severe global developmental delay and epilepsy.

      Patient 52 has generalized tonic/clonic/tonic-clonic seizures, focal seizures and spasms. Patient 52's seizure onset occurred at 3 months old.

      Patient 52 has cortical visual impairment (CVI), dystonia, chorea, and hand-washing sterotypies.

      Patient History

      @ 3 months - Patient 52 had generalized tonic/clonic/tonic-clonic seizures.

      Patient 52 was on 3 antiepileptic drugs at most recent follow-up visit which reduced seizure frequency by >50%.

      CaseNotHPOs:Not provided

      CaseNotHPOFreeText:Not provided

      CasePreviousTesting:The authors selected a cohort of 31 patients with seizure cryptogenic Neonatal/Infantile Epileptic Encephalopathy (NIEE) and seizure onset before 24 months.

      Exclusion criteria included: (1) Patients with a definite history of brain insult, malformation of cortical development, neurocutaneous and syndromal disorders, and confirmed or highly suspected neurometabolic disorders based on clinical and biochemical markers. (2) Patients with Dravet syndrome and epilepsy at infancy with migrating focal seizure were also excluded because the majority of variants are detected in the SCN1A (>85%) and KCNT1 (approximately 50%) genes.

      Formal neuropsychological testing or best clinical assessment was used to classify patient development or intelligence.

      PreviouslyPublished:Not previously published

      GenotypingMethod:Whole Exome Sequencing (WES) variant results were filtered in a panel of 430 epilepsy-associated genes. After selection of variants from the 430-gene panel, the synonymous variants, variants with variant frequency <10%, and variants with allele frequency >1% were removed.

      Gene:CDKL5

      Variant:NM_003159.2 c. 1849delC (p. Arg617Valfs*4)

      The authors state that the variant is a heterozygous frameshift deletion.

      The authors state that this is a novel variant and is pathogenic.

      HGVS:Not provided

      ClinVarID:Not found

      CAID:Not found.

      gnomAD:Not found

      MultipleGeneVariants:Not provided

    2. 7

      Case#:Patient 7, male, 5 years old

      DiseaseAssertion:Neonatal/Infantile Epileptic Encephalopathy (NIEE)

      FamilyInfo:The family is French/Chinese

      ParentalGenotype:The variant was inherited from Patient 7's asymptomatic mother.

      CasePresentingHPOs:HP:0010864, HP:0012758, HP:0000729, HP:0007359, HP:0002069, HP:0032794, HP:0001250, HP:0000252.

      CaseHPOFreeText:Patient 7 presents with severe intellectual disability, developmental slowdown, and various seizure types. Patient 7 has Autistic Spectrum Disorder (ASD) and microcephaly.

      Patient History

      @ 12 months - Patient 7 presented with seizures.

      Patient 7 developed additional seizure types including: focal seizures with/without generalization, generalized tonic/clonic/tonic-clonic seizures, myoclonic seizures, and hypomotor seizures.

      Patient 7 was on two antiepileptic drugs at most recent followup visit which reduced seizure frequency by >50%.

      CaseNotHPOs:Not provided

      CaseNotHPOFreeText:Not provided

      CasePreviousTesting:The authors selected a cohort of 31 patients with seizure cryptogenic Neonatal/Infantile Epileptic Encephalopathy (NIEE) and seizure onset before 24 months.

      Exclusion criteria included: (1) Patients with a definite history of brain insult, malformation of cortical development, neurocutaneous and syndromal disorders, and confirmed or highly suspected neurometabolic disorders based on clinical and biochemical markers. (2) Patients with Dravet syndrome and epilepsy at infancy with migrating focal seizure were also excluded because the majority of variants are detected in the SCN1A (>85%) and KCNT1 (approximately 50%) genes.

      Formal neuropsychological testing or best clinical assessment was used to classify patient development or intelligence.

      PreviouslyPublished:Not previously published

      GenotypingMethod:Whole Exome Sequencing (WES) variant results were filtered in a panel of 430 epilepsy-associated genes. After selection of variants from the 430-gene panel, the synonymous variants, variants with variant frequency <10%, and variants with allele frequency >1% were removed.

      Gene:SLC9A6

      Variant:Hemizygous splice site NM_001042537.1 c. 794-2A>G was assessed by the authors to be likely pathogenic.

      HGVS:Not provided

      ClinVarID:Not found

      CAID:CA414750320

      gnomAD:Not found

      MultipleGeneVariants:Not provided

    1. Case  1

      Case: Patient 1, female, 2 years old

      DiseaseAssertion: Rett Syndrome

      FamilyInfo: DeNovo. Patient 1 was the second child of a nonconsanguineous Chinese couple. Patient 1 was born at full term with a birth weight of 3.83 kg.

      ParentalGenotype(s):Not provided

      CasePresentingHPOs:HP:0011344, HP:0001250, HP:0001252, HP:0000252, HP:0000748, HP:0003763, HP:0005469, HP:0000486, HP:0012171.

      CaseHPOFreeRext:Patient 1 presents with severe global developmental delay, epilepsy, and hypotonia. The Patient History contains all of Patient 1's phenotypes along with the progression of her condition.

      Patient History

      @ 3 months - Patient 1 had microcephaly (head circumference was less than 3rd percentile with a body weight and body height at 75th percentile). Patient 1 had hypotonia.

      Patient 1 was given a metabolic screening, a muscle enzyme, and a brain tomography with normal results.

      @ 6 months - Patient 1 had microcephaly, flat occiput, right divergent squint, and hypotonia. No syndromal diagnosis could be ascertained at that time.

      @ 2 years - Patient 1 had epilepsy.

      Patient 1 had severe global development delay.

      Patient 1 was given an EEG which showed nonspecific background slowing, but no epileptiform abnormalities. Patient 1 was also given a brain MRI which showed mild thinning of corpus callosum without major structural defect. Patient 1 had no developmental regression but she developed stereotypical hand movements, bruxism, and occasional outburst of laughter.

      Based on these phenotypes, Angelman/Rett Syndrome was suspected.

      CaseNOTHPOs: HP:0002353.

      CaseNOTHPOFreeText: Patient 1 was given an EEG which detected no epileptic abnormalites.

      CasePreviousTesting: Genetic investigations (including methylation-specific multiplex ligation-dependent probe amplification (MS-MLLPA)) was conducted for Angelman Syndrome, UBE3A gene, MECP gene, and array CGH. These studies were negative. A FOXG1 related disease was suspected

      PreviouslyPublished:Not previously published

      GenotypingMethod: A FOXG1 gene test showed a de novo frameshift pathogenic mutation FOXG1 {NM_005249.3} c. 396_397ins26; FOXG1{NP_005240.3} :(p. Gly133TRPfs*68) which confirmed the diagnosis of a FOXG1 related congenital variant of Rett Syndrome.

      Gene:FOXG1

      Variant: (NM_005249.3) c. 396_397ins26 (p. Gly133Trpfs*68)

      HGVS:Not provided

      ClinVarID:Not found

      CAID:Not found

      gnomAD:Not found

    2. Case  2

      Case:Patient 2, female, Chinese

      DiseaseAssertion:Global delay

      FamilyInfo:Patient 2 was the first child of nonconsanguineous Chinese couple born at 38-week gestation. The mother had gestational diabetes mellitus that required insulin therapy.

      ParentalGenotype:Not provided

      CasePresentingHPOs:HP:0000365, HP:0020049, HP:0000252, HP:0001263, HP:0012171, HP:0000154, HP:0000708, HP:0003763, HP:0002376, HP:0012433.

      CaseHPOFreeText:

      Patient History

      @ birth - Patient 2 presented with mild grade bilateral hearing impairment and left divergent squint diagnosed at birth.

      @ Follow-up visit - Patient 2 had microbrachycephaly and global developmental delay. Brain MRI, metabolic screening and array CGH were normal.

      @ 1 year - Patient 2 had stereotypical handwashing movement.

      There was no clinical or electrical seizure.

      Patient 2 has craniofacial features like microbrachycephaly, wide mouth, divergent squint, and behavioral phenotype.

      @ 1.5 years - Patient 2 had bruxism and developmental regression. Patient 2 also had loss of some motor and social skills.

      CaseNotHPOs:HP:0001250

      CaseNotHPOFreeText:Patient 2 has no seizures.

      CasePreviousTesting:Not provided

      PreviouslyPublished:Not previously published

      GenotypingMethod:Not provided

      Gene:MECP2 (MN_004992.3) (NP_004983.1)

      Variant:c. 808C>T (p. Arg270*)

      HGVS:Not provided

      ClinVarID:Not found

      CAID:CA172577

      gnomAD:Not found

      MultipleGeneVariants:NA

    1. first patient

      Case:Patient 1, female, 11 years old

      DiseaseAssertion:Rett Syndrome - Atypical Variant

      FamilyInfo:De Novo. Patient 1's parents were healthy. When Patient 1 was clinically examined, the head circumferences of her mother and father were 53 cm (P25) and 59 cm (P90), respectively. The parents had normal weight.

      ParentalGenotype:Both parents were sequenced for Patient 1's mutation, and the deletion was not detected.

      CasePresentingHPOs:HP:0001249, HP:0001513, HP:0001626, HP:0000256, HP:0010465, HP:0012758, HP:0000750, HP:0012433, HP:0002591, HP:0001250, HP:0020174, HP:0000316, HP:0000336, HP:0000431, HP:0000377, HP:0000470, HP:0001156, HP:0001500.

      CaseHPOFreeText:

      Patient history

      @ birth - Patient 1 was born at 38 weeks of gestation after an uncomplicated pregnancy. Her weight was 3,390 g (P69), height 51 cm (P60), and her head circumference was 36 cm (P90).

      @ 6 months - Patient 1 experienced developmental delay.

      @ 9 months - Patient 1 sat without support.

      @ 2 years - Patient 1 began to walk.

      @ later on - Patient 1 presented with speech delay and behavioral disturbances. The behavioral disturbances were reduced by the drug risperidone.

      @ early childhood - Patient 1 has been obese and appeared to display hyperphagia.

      @ 8 years - Patient 1 developed precocious puberty.

      @ 10 years - Patient 1 had her first epileptic seizure. Treatment with lamotrigine prevented further seizures. The seizures later became refractory to this treatment.

      @ 10 years - Patient 1 presented with a height of 160 cm (P>97) and a head circumference of 59 cm (P>97). She had hypertelorism and prominent eyebrows. Her nasal bridge was broad and auricles were fleshy. In addition, Patient 1's neck was short and the fingers were short and wide.

      Patient 1 has an intellectual disability, metabolic syndrome, and macrocephaly.

      CaseNotHPOs:HP:0002540.

      CaseNotHPOFreeText:Patient 1 sat without support at 9 months old. She walked at 2 years.

      CasePreviousTesting:Patient 1 was given a conventional cytogenetic analysis. The chromosomal analyses (46,XX) and array CGH results (BlueGnome CytoChip ISCA 4×180K v1.0; Agilent Human Genome CGH Microarray 180K) were normal. Patient 1 was also given a methylation-specific MLPA to exclude a Temple syndrome, which is also characterized by weight gain and precocious puberty. In addition, Prader-Willi syndrome was ruled out by methylation testing. This syndrome is another imprinting disease causing obesity and intellectual disability.

      PreviouslyPublished:Not previously published

      GenotypingMethod:Whole-exome sequencing analysis of the entire exome was conducted for Patient 1. Whole-genome sequencing showed heterozygosity in Patient 1, which was confirmed by Sanger sequencing. Macrocephalic syndrome genes including PTEN, NSD1, NFIX, SETBP1, RAI1, and PHF6 were analyzed, and no additional variants of interest (pathogenic, likely pathogenic, or variants of uncertain significance) were observed.

      Gene:MECP2

      Variant:c. 1162_1172del (p. Pro388*), heterozygosity, frameshift.

      HGVS:NM_004992.3

      ClinVarID:Not found

      CAID:CA1139667881

      gnomAD:Not found

      MultipleGeneVariants:Not provided

    1. Patient 2

      Case:Patient 2, female, 2.5 years old

      DiseaseAssertion:CDKL5 Disorder

      FamilyInfo:De Novo with an unremarkable family history.

      ParentalGenotype:Not provided

      CasePresentingHPOs:HP:0032792, HP:0007359, HP:0011154, HP:0002194, HP:0010862, HP:0000750, HP:0012434, HP:0000710, HP:0100023, HP:0000252, HP:0009062, HP:0010845, HP:0020174, HP:0010841.

      CaseHPOFreeText:

      Patient history

      @ 2 months to 2.5 years - Patient 2 experienced tonic and focal seizures with autonomic symptoms.

      @ 2 years - Patient 2 was diagnosed with CDKL5 disorder.

      Patient 2 had severe delayed gross motor development, severe delayed fine motor development, severe delayed language development and delayed social development. Patient 2 had hyperoral and hand flapping stereotypies. She also had microcephaly (< 2 SD) and axial hypotonia.

      Patient 2 was given a brain EEG which detected Delta slowing of the background followed by generalized attenuation during seizures and multifocal interictal epileptiform abnormalities.

      @ 2.5 years - Patient 2 experienced seizures in clusters.

      Treatments

      Antiepleptic treatments included:Phenobarbital, Topirimate, Clobazam, Valproate, Keppra, Vitamin B6, Phenytoin, Lamotrigine, Nitrazepam, Oxcarbazepine, Mirtazipine, KCI, Levetiracetam, ant ketogenic diet.

      Patient 2 was also treated with Carnitine. Patient 2's seizures seem to have changed in type over time but continued.

      Other testing

      Tests were conducted on Patient 2 to obtain data in the following areas: NBS, lactate, lipoprotein profile, plasma and urine amino acids, urine organic acids, acylcarnitine profile, total and free serum carnitine levels, plasma ammonia, total plasma homocysteine, serum CK, liver enzymes, urine alpha-AASA, creatine, biotinidase, VLCFA, Batten disease screen, CSF analysis (amino acids, lactate, glucose, protein, cell count, neurotransmitters), MRI-brain with spectroscopy, and karyotype.

      CaseNotHPOs:Not provided

      CaseNotHPOFreeText:Not provided

      CasePreviousTesting:Patient 2 was given a gene sequence test for the genes SCNIA and MECP2. No gene mutation was found for these two genes.

      PreviouslyPublished:Not previously published

      GenotypingMethod:Patient 2 was given a CDKL5 gene sequence test. The test detected a mutation in the CDKL5 gene.

      Gene:CDKL5

      Variant:c. 2480_2486dupCAGATCT. frameshift

      The authors state that CDKL5 gene sequencing detected a de novo duplication in exon 17, c. 2480_2486dupCAGATCT, resulting in a frameshift (Boston University School of Medicine, Center for Human Genetics, Boston, MA). This is a novel change that has not been reported before in ExAC. Only pathogenic point mutations in exon 17 have previously been reported. In a patient with a previously reported frameshift mutation in exon 18, a truncated CDKL5 transcript was detected. A truncated protein would lack the C-terminus and would not localize correctly in the cell, as demonstrated in vitro. Accordingly, any reading frame altering mutations proximal to exon 18 are null-variants. Therefore, this mutation is classified as pathogenic according to ACMG criteria.

      HGVS:Not provided

      ClinVarID:547188

      NM_001323289.2 (CDKL5): c. 2480_2486dup (p. Gln830fs)

      Allele ID: 538303

      CAID:Not found

      gnomAD:Not found

      MultipleGeneVariants:Not provided

  2. Apr 2025
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  12. Dec 2023
      • annotate
      • for: evolutionary biology, big history, DH, Deep Humanity, theories of consciousness, ESP project, Earth Species Project, Michael Levin, animal communication, symbiocene

      • title: The Deep History of Ourselves: The Four-Billion-Year Story of How We Got Conscious Brains

      • author: Joseph LeDoux
      • date: Jan. 2023
      • doi: 0.1080/09515089.2022.2160311

      • ABSTRACT

        • The essence of who we are depends on our brains.
        • They enable us to think, to
          • feel joy and sorrow,
          • communicate through speech,
          • reflect on the moments of our lives, and to
            • anticipate,
            • plan for, and
            • worry about our imagined futures.
        • Although some of our abilities are comparatively new, key features of our behavior have deep roots that can be traced to the beginning of life.
        • By following the story of behavior, step-by-step, over its roughly four-billion-year trajectory,
          • we come to understand both
            • how similar we are to all organisms that have ever lived, and
            • how different we are from even our closest animal relatives.
        • We care about our differences because they are ours. But differences do not make us superior; they simply make us different.
      • comment

        • good article to contribute to a narrative of the symbiocene and a shift of humanity to belonging to nature as one species, instead of dominating nature as the apex species
      • question
        • @Gyuri, Could indranet search algorithm have made the connection between this article and the symbiocene artilces in my mindplex had I not explicitly made the associations manually through my tags? It needs to be able to do this
      • Also interesting to see how this materialistic outlook of consciousness
        • which is similiar to the Earth Species Project work and Michael Levin's work on synthesizing new laboratory life forms to answer evolutionary questions about intelligence
      • relates to nonmaterial ideas about consciousness
  13. Nov 2023
  14. Oct 2023
  15. Sep 2023
  16. Sep 2022
    1. This one is for students. Did you know you can annotate articles on Snapchat? Yes, it’s true!All you need to do is take a screenshot of the article you want to annotate.Then, open up the image editor and paste the article. Once you've done th

      What a watermeleon- I just made that up to say.

      Why did I not know this before... So I used to literally call out my students for Snap-chatting in class.

      If I knew about this educational use of Snap,, I would have used it already.

    2. Always make use of a key or legend when annotating articles online. A legend is a quick reference guide that explains what each symbol means.

      Wow! I taught this to my 9th graders. Why don't I apply it to my academics? Rhet

  17. May 2022
  18. Apr 2022
    1. often couldn’t quite track the notes I had taken on my readings or what they meant and, more often than not, I

      I think that the act of inscribing -- of adding the marginalia and of taking notes -- impresses upon the reader's memory.

  19. Mar 2022
    1. when it comes to storing and keeping track of what we’ve read in online spaces, we have to be attentive to the infrastructure(s) in which we encounter readings in the first place and we have to know how our practices may align (or clash) with those infrastructures.

      I have too many places with notes and annotations. I've been looking at Roam, Obsidian, and Databyss as places to aggregate my notes. Anyone else struggle to keep track of your annotations?

  20. Feb 2022
    1. When you read widely, your brain is exposed to different ways in which a sentence or paragraph is written. There are patterns in the use of nouns, pronouns, verbs and other parts of speech; there are patterns in syntax and in sentence variation; and there are patterns in sound devices, such as alliteration and assonance. You can annotate these with different symbols or colors, and develop understanding as patterns emerge, and style emerges from patterns. To read like a writer, you need to annotate like one, too.

      I haven't seen very much in the area of annotating directly as a means of learning to write. This is related to the idea of note taking for creating content for a zettelkasten, but the focus of such a different collection is for creating a writing style.

      Similar to boxing the boring words (see Draft #4; http://jsomers.net/blog/dictionary), one should edit with an eye toward the overall style of a particular piece.


      Annotating structures and patterns in books is an interesting exercise to evaluate an author's style as a means of potentially subsuming, modifying, or learning other styles.

  21. Mar 2021
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  23. Dec 2020
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  28. Mar 2019
    1. They lie there stretched out by the captive roads, along the ………..roads of disaster The lean poplars, the statues of the dark gods ………..draped in their long gold coats Senegalese prisoners miserably lying ………..on the French land.

      In vain they cut your laughter, in vain the blacker the flower, the ………..blacker your flesh. You are the flower of beauty among the first absence ………..nude flowers Black flower blossom and its somber smile, diamond of a time ………..immemorial. You are the mud and plasma of the world’s leafy ………..spring From the primitive couple, you are the flesh of the womb, the ………..belly fertilizing milt You are the sacred profusion of bright, blissful gardens And the sovereign forest, victorious of fire and lightning

      The vast song of your blood will defeat machines and canons Your speech throbbing deceptions and lies No hate in your soul, you are not hateful, no cunning ………..soul without cunning. O Black Martyrs, immortal race, let me say the ………..words that forgive.

  29. Oct 2018
    1. This allowed for the examination of the accuracy of the four groups com-pared to the accuracy obtained by luck or simple knowledge of the social ste-reotype of the typical murder.

      why is the control group random people? :/

  30. Mar 2018
  31. Oct 2017
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  33. Jun 2016
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  35. Mar 2015