36 Matching Annotations
  1. Last 7 days
    1. 3746Fnt 712 C to T, Arg to TrpP, 16016

      PatientID: 37

      KindredID: 6016

      Case: F, 46Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0030405 (pancreatic endocrine tumour)

      CaseHPOFreeText: She presented with one pathologic pancreatic endocrine tumour.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.R167W (c.499C>T)

      LegacyVariant: p.R167W (c.712C>T)

      CaseProblemVariantFreeText: N/A

      ClinVar: 2218 https://www.ncbi.nlm.nih.gov/clinvar/variation/2218/

      CAID: CA020450 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.499C%3ET

      gnomAD: 0.000007954 https://gnomad.broadinstitute.org/variant/3-10191506-C-T

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: R167W (c.499C>T)

      MultipleGeneVariants: N/A

    1. PatientID: 2288

      KindredID: 65

      Case: Sex Unknown, Age Unknown, French

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CohortInfo: Families were recruited from the French VHL Registry. Enrolment in the study required identification of the germline VHL mutation (currently 85% of the families included in the French VHL Registry) and available data regarding renal phenotype. A total of 126 families fulfilled these criteria.

      CasePresentingHPOs: HP:0005584 (Renal cell carcinoma)

      CaseHPOFreeText: Severe renal disease (any solid lesion before 25 years of age, five or more solid lesions within one or two kidneys, or metastasis of renal cell carcinoma). Individual RCC phenotype is noted as positive.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 12202531

      SupplementalData: Phenotype and genotype information can be found in Supplementary Table S1.

      Variant: p.E46* (c.136G>T)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA351748085, https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.136G%3ET

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion; stop_gained

      CivicName: E46* (c.136G>T)

      MultipleGeneVariants: N/A

    1. Our series comprised 125 eligible subjects with germlineVHL c.505 T/C mutation, including 64 previously known and 61 newly diagnosed mutation carriers.

      GroupID: None

      DiseaseAssertion: VHL

      GroupSize: 125

      GroupNumberMales: 58

      GroupNumberFemales: 67

      GroupEthnicity: German

      GroupAgeRange: 4-86 Y

      GroupInfo: The subjects included 64 patients belonging to 15 families with a known VHL c.505 T/C mutation. From their test programme, another 10 c.505 T/C mutation carriers were identified. As well, all consenting first degree relatives (at risk subjects) of mutation carriers, irrespective of disease status, were subjected to mutation analysis, resulting in another 51 mutation carriers detected.

      GroupPresentingHPOs: HP:0002666, HP:0009713, HP:0009711, HP:0010797, HP:0006748, HP:0006737, HP:0006770, HP:0002893, HP:0100616, HP:0030357, HP:0002894 (pheochromocytoma, spinal hemangioblastoma, retinal capillary hemangioma, hemangioblastoma, adrenal pheochromocytoma, extraadrenal pheochromocytoma, clear cell renal cell carcinoma, pituitary adenoma, testicular teratoma, small cell lung carcinoma, neoplasm of the pancreas)

      GroupHPOFreeText: 96 patients had clinical manifestations of VHL. 55 subjects (31 males, 24 females) developed pheochromocytoma during their lifetime. Overall penetrance for pheochromocytomas was estimated to be 31% by age 35 and 60% by age 70. Other frequent lesions were retinal angioma (36%), hemangioblastoma of the spine (36%), and, to a lesser extent, hemangioblastoma of the brain (16%). One patient with angiomatosis retinae developed at least 25 retinal angiomas, whereas the remaining patients had an average of two angiomas with no more than five lesions in one patient. 15 patients had bilateral and 25 unilateral involvement of the retinae. Pheochromocytoma was observed as a single tumour with adrenal or extra-adrenal localization in 32 patients, but 23 mutation carriers developed multiple pheochromocytomas. Four patients developed renal clear cell carcinoma (estimated overall penetrance 13% by the age of 70). Two of these patients died of metastases. All renal clear cell carcinomas were unilateral, single tumours, and no kidney showed renal cysts. Three of the patients with renal cell carcinoma were female. The kidney tumours were detected at the ages of 46 (male patient), 48, 63, and 74 years. Two patients with renal cell carcinoma also had multiple spinal hemangioblastomas. Other rare tumours were one pancreatic islet cell tumour and one pituitary adenoma; both neoplasms had been incidentally found in a dead 34 year old woman at necropsy. One 68 year old male patient was noted to have small cell lung cancer, and two other males developed testicular teratocarcinoma both at 39 years of age.

      GroupNotHPOs: N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.Y98H (c.292T>C)

      LegacyVariant: p.Y98H (c.505T>C)

      CaseProblemVariantFreeText: N/A

      ClinVarID: 2223 https://www.ncbi.nlm.nih.gov/clinvar/variation/2223/

      CAID: N/A

      gnomAD: 0.00001343 https://gnomad.broadinstitute.org/variant/3-10183823-T-C

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: Y98H (c.292T>C)

      MultipleGeneVariants: N/A

    1. In family 4, the proband was a female who had a bilateral pheochromocytoma at the age of 46 years that recurred locally with liver metastases a few years later. Her brother had a monolateral benign pheochromocytoma. The proband also had a melanoma and bilateral renal cysts. A VHL sequence variant IVS2 +43 A>G was found in this case and also in one other unrelated sporadic pheochromocytoma. Their VHL mRNA integrity is currently being assessed. The proband had no cerebellar or spinal NMR finding or retinal alterations. Molecular analysis showed the following sequence variants: VHL IVS2 +43 A>G, RET c.2071 G>A p.G691S, SDHD c.34 G>A p.G12S, IVS2-29 A>G, c.204 C>T p.S68S, and IVS3-32 T>C.

      PatientID: 4 (proband)

      KindredID: 4

      Case: F, 46Y0M, Ethnicity Unknown

      DiseaseAssertion: assumed VHL

      FamilyInfo: Positive family history with her brother having a monolateral benign pheochromocytoma

      CasePresentingHPOs: HP:0002666; HP:0002861; HP:0000107 (pheochromocytoma; melaonoma; renal cyst)

      CaseHPOFreeText: Bilateral pheochromocytoma at the age of 46Y with a local reccurance a few years later. She also presented with liver metastases from the pheochromocytoma, as well as melanoma and bilateral renal cysts

      CaseNotHPOs: (HP:0006880; HP0009713; HP:0009711)

      CaseNotHPOFreeText: She had no cerebellar or spinal hemangiostaomasm nor retinal alterations

      CasePreviousTesting: RET/SDHB/SDHC/SDHD/EGLN3

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: c.463+43A>G

      LegacyVariant: IVS1+43A>G

      CaseProblemVariantFreeText: N/A

      ClinVarID: 1244574 https://www.ncbi.nlm.nih.gov/clinvar/variation/1244574/

      CAID: N/A

      gnomAD: 0.01186 https://gnomad.broadinstitute.org/variant/3-10188363-A-G

      VariantEvidence: this intronic sequence variant may have a role in VHLd because it was also detected in this study in a case of sporadic pheochromocytoma. However, this variant’s large allele frequency means this is likely non disease causing (not deleterious; polymorphism).

      MutationType: splice_site_variant; intron_variant

      CivicName: c.463+43A>G

      MultipleGeneVariants: Germline, RET, c.2071G>A (p.Gly691Ser); Germline, SDHD, c.34G>A (p.Gly12Ser); SDHD, (IVS2-29A>G); SDHD c.204C>T (p.Ser68Ser); SDHD (IVS3-32T>C)

    1. a case

      PatientID: None

      KindredID: 1

      Case: M, 66Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: The patient’s elder sister died of a cerebellar tumor of unknown pathology at 30Y. As well, the patient’s son presented with cerebellar hemangioblastoma and was diagnosed with VHL disease.

      CasePresentingHPOs: HP:0002666; HP:0006880; HP:0100009; HP:0005584 (Pheochromocytoma, cerebellar hemangioblastoma, intracranial meningioma, renal cell carcinoma)

      CaseHPOFreeText: The 66Y male patient presented with mild dementia, and was found to have multiple tumours in the cerebellum; the tumours were resected, and histological examination determined that the tumours included meningothelial meningioma and a capillary hemangioblastoma. The patient was also found to have renal cell carcinoma, and underwent nephrectomy. The patient had also previously undergone resection for a giant pheochromocytoma associated with malignant hypertension 20 years prior at 46Y. The patient died of multiple cerebral infarctions and RCC three years after the surgery to remove the cerebellar tumours.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.L158V(c.472C>G)

      LegacyVariant: p.L158V(c.685C>G)

      ClinVarID: 567944, https://www.ncbi.nlm.nih.gov/clinvar/variation/567944/

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName: L158V(c.472C>G)

      MultipleGeneVariants: N/A

  2. Nov 2026
    1. PatientID: 237

      KindredID: 89

      Case: F, 46Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0005584 (Renal cell carcinoma)

      CaseHPOFreeText: The proband presented with renal cell carcinoma at age 46.

      CaseNotHPOs: HP:0010797; HP:0002666; HP:0009711; HP:0001737; HP:0001732 (Hemangioblastoma, Pheochromocytoma, Retinal capillary hemangioma, Pancreatic cysts, Abnormality of the pancreas)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: This patient was also published in a later paper by Wang et al., 2018 (PMID: 29330336).

      SupplementalData: Patient and family genotype-phenotype information is listed in Supplementary Table 1.

      Variant: c.642+70C>T

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 900551, https://www.ncbi.nlm.nih.gov/clinvar/variation/900551/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: splice_site_variant

      CivicName: 3'UTR alteration (c.*70C>T)

      MultipleGeneVariants: N/A

  3. Oct 2026
    1. PatientID: 252

      KindredID: 97

      Case: M, 46Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0010797; HP:0009711; HP:0001737; HP:0001732; HP:0005584 (Hemangioblastoma, Retinal capillary hemangioma, Pancreatic cysts, Abnormality of the pancreas, Renal cell carcinoma)

      CaseHPOFreeText: The patient presented with a CNS hemangioblastoma, retinal angioma, renal cell carcinoma, and multiple pancreatic cysts/tumors at age 46.

      CaseNotHPOs: HP:0002666 (Pheochromocytoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: This cohort was also published in a later paper by Wang et al., 2018 (PMID: 29330336).

      SupplementalData: Patient and family genotype-phenotype information is listed in Supplementary Table 1.

      Variant: Exon 1 Deletion (c.1-?_340+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 1 Deletion

      MultipleGeneVariants: N/A

    2. PatientID: 208

      KindredID: 79

      Case: M, 49Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: The proband's mother and sister had a CNS hemangioblastoma at ages 40 and 50, respectively. His nephew presented with a CNS hemangioblastoma (age 15), a retinal angioma (age 27), and renal cell carcinoma (age 25). His daughter had a retinal angioma at age 14, and a CNS hemangioblastoma at age 24. No genetic testing information was available for family members.

      CasePresentingHPOs: HP:0010797; HP:0001737; HP:0001732; HP:0002666; HP:0005584 (Hemangioblastoma, Pancreatic cysts, Abnormality of the pancreas, Pheochromocytoma, Renal cell carcinoma)

      CaseHPOFreeText: The proband presented with a CNS hemangioblastoma at age 29. At age 46, they presented with renal cell carcinoma and a pheochromocytoma. At age 49 they presented with multiple pancreatic cysts/tumors.

      CaseNotHPOs: HP:0009711; (Retinal Capillary Hemangioma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: Kindred #79 was published in Wang et al., 2014 (PMID: 24581539). This cohort was also published in a later paper by Wang et al., 2018 (PMID: 29330336).

      SupplementalData: Patient and family genotype-phenotype information is listed in Supplementary Table 1.

      Variant: p.R167Q (c.500G>A)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 2216, https://www.ncbi.nlm.nih.gov/clinvar/variation/2216/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: R167Q (c.500G>A)

      MultipleGeneVariants: N/A

    1. In 1994, a 34-yr-old woman without personal and familial history for VHL was referred to the hospital because of persistent pharyngeal discomfort. MRI demonstrated a 4-cm tumor in the parapharyngeal space suggestive of a schwannoma or a carotid paraganglioma. The tumor was removed, and histology revealed a paraganglioma. Postoperatively, she had Horner’s syndrome and a transitory hypoglossal paresis. At age 46, bilateral adrenal pheochromocytoma and a paraaortic paraganglioma were removed. Later, her niece was diagnosed with a pheochromocytoma, and her brother suffered from pheochromocytoma, renal cell carcinoma, and retinal hemangioblastomas. The proband’s mother was then found to have pheochromocytoma. Molecular analysis identified the VHL mutation p.Tyr98His.

      PatientID: 10

      KindredID: 10

      Case: F, 46Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: The patient's niece was diagnosed with a pheochromocytoma, her brother suffered from pheochromocytoma, renal cell carcinoma, and retinal hemangioblastomas, and her mother was found to have pheochromocytoma.

      CohortInfo: An international consortium registered patients with head and neck paragangliomas with VHL or RET gene mutations.

      CasePresentingHPOs: HP:0002864, HP:0002277, HP:0006748 (Paraganglioma of head and neck, Horner syndrome, adrenal pheochromocytoma)

      CaseHPOFreeText: At age 34 the patient was found to have a 4-cm tumor in the parapharyngeal space. It was histologically confirmed to be a paraganglioma. Postoperatively, she had Horner’s syndrome and a transitory hypoglossal paresis. At age 46, bilateral adrenal pheochromocytoma and a paraaortic paraganglioma were removed.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: RET

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.Y98H (c.292T>C)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 2223 https://www.ncbi.nlm.nih.gov/clinvar/variation/2223/

      CAID: N/A

      gnomAD: 0.00001343 https://gnomad.broadinstitute.org/variant/3-10183823-T-C

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: Y98H (c.292T>C)

      MultipleGeneVariants: N/A

    1. 136G→T Ts Exon 1 46 GAG E E46X

      GroupID: 1

      Case: Age unknown, Sex unknown, French

      DiseaseAssertion: VHL

      FamilyInfo: None - one member documented here

      CasePresentingHPOs: HP:0009711 (retinal capillary hemangioma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: Possibly published in PMID:15300849

      SupplementalData: N/A

      Variant: p.E46* (c.136G>T)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: CA351748085 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.136G%3ET

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: stop_gained

      CivicName: E46* (c.136G>T)

      MultipleGeneVariants: N/A

    1. Interestingly, one carrier of the deletion developed bilateral breast cancer at age 46 and 49. First cancer was diagnosed at the age of 46 in her right breast. The patient was treated by mastectomy with postoperative chemotherapy (CMF). Histopathological examination revealed invasive ductal breast carcinoma of 1.8 cm size. The tumor was ER- negative, and PR-negative (HER2 was not analyzed). A metastasis in 1 axillary lymph node was found. There was no evidence of distant metastases. The tumor was classified as T1c pN1a M0, stage IIA; grade G2. Three years later, at the age of 49, she was diagnosed with cancer of her left breast. It was an invasive ductal carcinoma of 2.0 cm size. The tumor was ER-positive, PR-positive, and HER2-negative. There was no evidence for lymph-node or distant metastases. The tumor was classified as T1c pN 0 M0, stage IA, grade G2 and treated with mastectomy and tamoxifen. Ki67 expression was not tested. At present, 9 and 6 years after treatment of the breast cancers there is no evidence of breast cancer recurrence. However at age of 54, lesions typical for VHL disease including cerebellar haemangioblastoma and renal cell carcinoma were diagnosed in the patient.

      PatientID: 2

      KindredID: 1

      Case: F, 54Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: Son (id:1) with the same variant, presenting with cerebellar hemangioblastoma at age 18, spinal hemangioblastomas at ages 19 and 31 and renal cysts but the age of onset for these is not noted. Father (id: 3) presented with cerebellar hemangioblastoma at age 65. Paternal uncle (id: 4) presented with prostate cancer at age 65. Paternal grandfather (id: 5) presented with cerebellar hemangioblastomas at age 69. Mother and daughter did not have the mutation. Her father was not tested. No family history of retinal capillary hemangiomas or pheochromocytoma.

      CasePresentingHPOs: HP:0006880; HP:0005584; HP:0003002 (Cerebellar hemangioblastoma, Renal cell carcinoma, Breast carcinoma)

      CaseHPOFreeText: Bilateral breast cancer at age 46 and 49. First cancer was diagnosed at the age of 46 in her right breast. The patient was treated by mastectomy with postoperative chemotherapy (CMF). Histopathological examination revealed invasive ductal breast carcinoma. A metastasis in 1 axillary lymph node was found. There was no evidence of distant metastases. Three years later, at the age of 49, she was diagnosed with cancer of her left breast. It was an invasive ductal carcinoma. There was no evidence for lymph-node or distant metastases. At present, 9 and 6 years after treatment of the breast cancers there is no evidence of breast cancer recurrence. However at age of 54, lesions typical for VHL disease including cerebellar haemangioblastoma and renal cell carcinoma were diagnosed in the patient.

      CaseNotHPOs: HP:0002666; HP:0009711 (Pheochromocytoma, Retinal capillary hemangioma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Figure 1 (pedigree) and Table 1 (phenotype and age of onset data).

      Variant: Exon 1 Deletion (c.1-?_340+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 1 Deletion

      MultipleGeneVariants: Germline, FANCD2, Partial Deletion

  4. May 2026
    1. That Pigeon Looks Just Like Michael Keaton<br /> The Late Show with Stephen Colbert

      Definitely a late model Olivetti. Either a Studio 45, which was more common in the United States, or a Studio 46, both of which came in that color.

      I'm leaning toward 46 because of some of the shape of the hood as well as the white variable button on the platen which I've only ever seen on the 46 while the 45s were typically black or had the button colored to match the body color.

  5. Aug 2025
    1. Reply to Joe Van Cleave at https://typewriterdatabase.com/show.21270.typewriter

      It's probably a subtle difference, but is this machine provide the standard 6 lines per vertical inch or due to the taller ascenders/descenders is it a 4 lines per vertical inch machine?

      If you need a "name" for this machine, I might suggest "Satchmo". In doing some research on Louis Armstrong's 5 series Smith Corona, I'm pretty sure his 5 series also had this same vertical script. None of the features on any of the photos I could find of his machine are subtle enough to distinguish which particular model of Smith-Corona he was using. If we find a good direct photo of the machine itself, I'm sure I could puzzle out which version he used. By 1955 he had at least one machine with a script face (see: https://www.louisarmstronghouse.org/virtual-exhibits/my-fifty-fifth-birthday-celebration-happy-birthday-louis-armstrong/). It doesn't appear to be Smith-Corona's common Script (Artistic) No. 75 , but more like Script No. 46. Based on a version of this photo (https://www.usatoday.com/gcdn/presto/2019/07/15/USAT/d815dddc-c0b8-4c54-b9b5-719886d4a0cc-02_Armstrong_Louis_16.jpg?width=1292&height=1320&fit=crop&format=pjpg&auto=webp) it would seem that it's the Smith-Corona that was the script machine (as opposed to his earlier Remington).

      According to Ted Munk's post on the S-C Vertical script: "Smith Corona is offering the [vertical] typeface as 'Script No. 46', 10 Pitch by 1954."

      Joe's video of his 1952 Smith-Corona this with the same vertical script https://www.youtube.com/watch?v=EH6mwmoN_LI

      See also: https://www.reddit.com/r/typewriters/comments/1mo4wbg/what_typewriter/

      Somewhat interesting that Louis Armstrong played cornet, wrote on a Smith-Corona, and lived in the Corona neighborhood of Queens, NY.

  6. Mar 2025
    1. KoponewtPelicram ❤️ Slug Goblin 3 points4 points5 points 3 hours ago (3 children)Do you know what's the serial number on that? Some manufacturers had special models mostly for export purposes with extra keys. For example Royal 11 is a 10 with extra keys, Underwood No. 46 is a 5/3/6 with extra keys. Remington No. 9 is an 8 with extra keys.

      via https://old.reddit.com/r/typewriters/comments/1jgg4kh/royal_kmm_extra_column_of_keys/miyumvn/

  7. Dec 2024
  8. Jun 2024
  9. Feb 2023
    1. section 702 is compulsory in the sense that, when the United States hasissued a directive to an electronic communication service provider that is authorizedby its annual certification to the FISA Court under section 702, the provider musteither (1) comply; or (2) challenge the directive in the FISA Court

      FISA 702 Orders are compulsory - you either comply, or challenge.

    1. Such instruments should, forexample, address the measures to be taken in case of conflict of laws between third country legislationand the GDPR and in the event of third country requests for disclosure of data.

      But how? in the DPA? The point of the transfer mechanism (e.g., SCCs / BCRs) is to be standard. You can't modify them.

      This sounds like a thing the EDPB/EC need to do not controllers/processors directly.

  10. Apr 2021
    1. Quelques textesArticle R. 421-46 du code de l’éducation«Le comité d'éducation à la santé et à la citoyenneté réunit, sous la présidence du chefd'établissement, les personnels d'éducation, sociaux et de santé de l'établissement et desreprésentants des personnels enseignants, des parents et des élèves, désignés par le chefd'établissement sur proposition des membres du conseil d'administration appartenant à leurscatégories respectives, ainsi que les représentants de la commune et de la collectivitéterritoriale de rattachement au sein de ce conseil. En fonction des sujets traités, il peutassocier à ses travaux toute personne dont il estime l'avis utile»
  11. Mar 2021
    1. Results for individual PALB2 variants were normalized relative to WT-PALB2 and the p.Tyr551ter (p.Y551X) truncating variant on a 1:5 scale with the fold change in GFP-positive cells for WT set at 5.0 and fold change GFP-positive cells for p.Y551X set at 1.0. The p.L24S (c.71T>C), p.L35P (c.104T>C), p.I944N (c.2831T>A), and p.L1070P (c.3209T>C) variants and all protein-truncating frame-shift and deletion variants tested were deficient in HDR activity, with normalized fold change <2.0 (approximately 40% activity) (Fig. 1a).

      AssayResult: 6.2

      AssayResultAssertion: Normal

      StandardErrorMean: 1.39

    1. Most Suspected Brugada Syndrome Variants Had (Partial) Loss of Function

      AssayResult: 1.6

      AssayResultAssertion: Abnormal

      ReplicateCount: 15

      StandardErrorMean: 0.7

      Comment: This variant had loss of function of peak current (<10% of wildtype), therefore it was considered abnormal (in vitro features consistent with Brugada Syndrome Type 1). (Personal communication: A. Glazer)

  12. Feb 2021
  13. Feb 2019