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  1. Last 7 days
    1. frameshift mutations (4/16)

      PatientID: 12

      KindredID: 12

      Case: 32Y0M, Sex Unknown, Argentinian

      DiseaseAssertion: VHL

      FamilyInfo: Family history unremarkable; Patient was confirmed to have a de novo mutation.

      CasePresentingHPOs: HP:0010797; HP:0009711; HP:0000107; HP:0030424 (hemangioblastoma; retinal capillary hemangioma; renal cyst; epididymal cyst)

      CaseHPOFreeText: Aged 32Y at diagnosis (genetic testing); fulfils type 1 VHL clinical diagnosis. Retinal hemangioblastomas and CNS hemangioblastomas diagnosed at 32Y, renal cysts were also diagnosed at 32Y, while epididymal cysts were diagnosed first at 23Y (See Table 1 & 2).

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.V74Sfs*53 (c.219_232delGGTCATCTTCTGCA)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA2497423672 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/by_caid?caid=CA2497423672

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: minus_2_frameshift_variant

      CivicName: V74Sfs*53 (c.219_232delGGTCATCTTCTGCA)

      MultipleGeneVariants: N/A

    1. 1 (100)

      GroupID: 10

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: VHL

      CohortInfo: a retrospective cohort study from an eye centre in Germany involved 148 VHL patients and their genetic data involved in retinal capillary hemangiomas.

      CasePresentingHPOs: N/A

      CaseHPOFreeText: This individual patient did NOT have retinal capillary hemangiomas. Other VHL manifestations were discussed but not per- variant.

      CaseNotHPOs: HP:0009711 (retinal capillary hemangioma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Yes - Supplementary Table S1

      Variant: p.F136Lfs*23 (c.408delT)

      LegacyVariant: N/A

      GroupProblemVariantFreeText: N/A

      ClinVarID: 43601 https://www.ncbi.nlm.nih.gov/clinvar/variation/43601/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: minus_1_frameshift_variant

      CivicName: F136LFS*23 (c.408del)

      MultipleGeneVariants: N/A

    1. Case 1: Clinical historyA 25-year-old woman presented with a 1-year history of slowly progressive and gradual decrease in hearing. Two years previously, the patient had undergone brain surgery because of hemangioblastoma of the cerebellum. Gene analysis performed at that time showed mutation in VHL gene in exon 1 TCG(Ser65)→TTG(Leu). On physical examination, she was found to have a middle ear mass that protruded into the external auditory canal. Bone destruction was found radiographically. At surgery, vascular tumor tissue and cysts were seen permeating and destroying the adjacent petrous portion of the temporal bone with invasion of the mastoid and the semicircular canal. The patient underwent a complete removal of the tumor from the middle ear, mastoid, and petrous bone. However, recurrent destructive tumor of the middle ear appeared after 26 months.Family historyThe family medical history disclosed the presence of symptoms of VHLD in the patient's grandfather, uncle, and father. In particular, the patient's father presented with multi-tumor syndrome and evidence of genetic VHLD due to causal mutation in VHL gene in exon 1 TCG(Ser65)→TTG(Leu). At the age of 30, he was operated on for cerebellar hemangioblastoma, and died of disseminated bilateral renal cell carcinoma of kidneys with multi-organ distant metastases 13 years later at the age of 43.

      PatientID: 1

      KindredID: 1

      Case: F, 25Y0M, Ethnicity Unknown

      DiseaseAssertion: assumed VHL

      FamilyInfo: The family medical history disclosed the presence of symptoms of VHLD in the patient’s grandfather, uncle, and father. In particular, the patient’s father presented with multi-tumor syndrome and a confirmed genetic mutation of c.194C>T. The father died of disseminated bilateral renal cell carcinoma of kidneys with multi-organ distant metastases at the age of 43.

      CasePresentingHPOs: HP:0006880;HP:0030393 (cerebellar hemangioblastoma, endolymphatic sac tumour)

      CaseHPOFreeText: Woman presented with slowly progressive and gradual decrease in hearing (beginning at 24Y). At 23Y the patient had undergone brain surgery because of hemangioblastoma of the cerebellum. Physical examination revealed a middle ear mass that protruded into the external auditory canal (recurrent restrictive tumor)

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.S65L (c.194C>T)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 182975, https://www.ncbi.nlm.nih.gov/clinvar/variation/182975/

      CAID: N/A

      gnomAD: https://gnomad.broadinstitute.org/variant/3-10183725-C-T

      VariantEvidence: genetic tests on tissue but suspected germline because father had same mutation, and 2 different tissue samples had same mutation; grandfather and uncle had VHL symptoms but not specified and no genetic confirmation

      MutationType: missense_variant;transition

      CivicName: S65L (c.194C>T)

      MultipleGeneVariants: N/A

    1. Family 4−1c.275insCCdelAYes123––24––

      PatientID: None

      KindredID: 4

      Case: Unknown, 24Y0M, Chinese

      DiseaseAssertion:VHL

      FamilyInfo: None.

      CasePresentingHPOs: HP:0010797, HP:0001732 (hemangioblastoma, abnormality of the pancreas)

      CaseHPOFreeText:The patient presented with hemangioblastoma at age 23. One year later he/she was found to have pancreatic cysts or tumors.

      CaseNotHPOs: HP:0009711, HP:0002666, HP:0005584 (retinal capillary hemangioma, pheochromocytoma, renal cell carcinoma)

      CaseNotHPOFreeText: No epididymal/ovarian cystadenomas.

      CasePreviousTesting: N/A

      PreviouslyPublished: 29330336

      Variant: p.D92Afs*40(c.275delAinsCC)

      LegacyVariant:N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA1139768933 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.275delAinsCC

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: delins

      CivicName:D92fs(c.275delAinsCC)

      MultipleGeneVariants: N/A

    1. Grand cousin 1–22–23Renal cysts

      PatientID: None (Grand Cousin 1)

      KindredID: G

      Case: Sex Unknown, 23Y0M, Hungarian

      DiseaseAssertion: Assumed VHL

      FamilyInfo: Large VHL family spanning five generations. The index patient presented with pheochromocytoma, renal cell carcinoma as well as spinal cord, cerebellar, and medulla oblongata hemangioblastomas. Her parents showed no clinical, biochemical, or radiological evidence of the disease, but VHL-associated tumors were detected in five other family members (bilateral renal cell carcinomas in one, renal cysts in one, spinal cord, cerebellar, and medulla oblongata hemangioblastomas in three, retinal hemangioblastomas in four, and pheochromocytomas in two family members).

      CasePresentingHPOs: HP:0010797; HP:0009711; HP:0005562 (Hemangioblastoma, Retinal capillary hemangioma, Multiple renal cysts)

      CaseHPOFreeText: Presented with CNS hemangioblastoma at age 22 and retinal hemangioblastoma at age 23. No VHL diagnosis noted but assumed to have VHL based on genetic, clinical and familial findings.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 18416845

      SupplementalData: N/A

      Variant: p.S80I (c.239G>T)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 625229, https://www.ncbi.nlm.nih.gov/clinvar/variation/625229/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Variant reported as S80I and cDNA change was mapped to c.239G>T.

      MutationType: missense_variant;transversion

      CivicName: S80I (c.239G>T)

      MultipleGeneVariants: N/A

    1. PatientID: S-V1

      KindredID: S-V1

      Case: M, 48Y0M, Korean

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0005584; HP:0005562 (Renal cell carcinoma, Multiple renal cysts)

      CaseHPOFreeText: Bilateral RCC and multiple renal cysts. Diagnosed with VHL type 1.

      CaseNotHPOs: HP:0010797; HP:0002666 (Hemangioblastoma, Pheochromocytoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 25078357

      SupplementalData: N/A

      Variant: p.R108Hfs*23 (c.323_324del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA916832609, https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/by_canonicalid?canonicalid=CA916832609

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: deletion; minus_2_frameshift_variant

      CivicName: R108Hfs*23 (c.323_324del)

      MultipleGeneVariants: N/A

    1. GroupID: 61

      Case: Age Unknown, Sex Unknown, Ethnicity Unknown

      DiseaseAssertion: assumed VHL

      FamilyInfo: 1 of the 573 patients discussed in this paper were found to have this variant. This mutation (c.262T>A) was found in 1 VHL family with a single patient.

      CasePresentingHPOs: HP:0005584; HP:0009711; HP:0006880 (renal cell carcinoma; retinal capillary hemangioma; cerebellar hemangioblastoma)

      CaseHPOFreeText: patient had retinal angioma diagnosed at 23Y, cerebellar hemangioblastoma diagnosed at 54Y, and RCC at 54Y.

      CaseNotHPOs: HP:0002666 (pheochromocytoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplementary Table S1.

      Variant: p.W88R (c.262T>A)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 456577 https://www.ncbi.nlm.nih.gov/clinvar/variation/456577/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName: W88R (c.262T>A)

      MultipleGeneVariants: N/A

    1. PatientID: 23

      KindredID: 23

      Case: M, 48Y0M, Korean

      DiseaseAssertion: VHL

      FamilyInfo: No family history of VHL.

      CohortInfo: 26 Korean patients with more than one HAB in the CNS or eye, a single HAB in the CNS or retina plus a visceral manifestation (multiple renal, pancreatic or hepatic cysts, pheochromocytoma and RCC) and positive family history plus any one of the above manifestations.

      CasePresentingHPOs: HP:0005584 (Renal cell carcinoma)

      CaseHPOFreeText: Multiple or bilateral renal cell carcinoma. Other phenotypes presented but not specified (one or more of: pancreatic cyst or tumor, renal or hepatic cyst). Diagnosed with VHL Type 1. Phenotypes revised from previous reports (see “PreviouslyPublished” section below for PMID).

      CaseNotHPOs: HP:0009711; HP:0002666; HP:0010797 (Retinal capillary hemangioma, Pheochromocytoma, Hemangioblastoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 16142346

      SupplementalData: N/A

      Variant: p.R108Hfs*23 (c.323_324del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA916832609, https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/by_canonicalid?canonicalid=CA916832609

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: deletion; minus_2_frameshift_variant

      CivicName: R108Hfs*23 (c.323_324del)

      MultipleGeneVariants: N/A

    1. 17 (22%) had frameshift variants

      PatientID: 66

      KindredID: 66

      Case: Sex, Age, Ethnicity unknown

      DiseaseAssertion: VHL (asymptomatic)

      FamilyInfo: N/A

      CasePresentingHPOs: N/A

      CaseHPOFreeText: N/A

      CaseNotHPOs: HP:0030421; HP:0009711; HP:0030405; HP:0006770; HP:0100634; HP:0010797 (epididymal tumour, retinal capillary hemangioma, pancreatic endocrine tumour, clear cell renal cell carcinoma, neuroendocrine neoplasm, hemangioblastoma)

      CaseNotHPOFreeText: patient was not recorded to have an epididymal tumor, a pancreatic endocrine tumour (pancreatic neuroendocrine neoplasm), CCRCC, a neuroendocrine neoplasm (pheochromocytoma/paraganglioma), nor a CNS hemangioblamstoma.

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Yes; see table S1 for VHL subject genetic and manifestation information.

      Variant: p.F136Lfs*23 (c.408delT)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 43601 https://www.ncbi.nlm.nih.gov/clinvar/variation/43601/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: minus_1_frameshift_variant

      CivicName: F136Lfs*23 (c.408delT)

      MultipleGeneVariants: N/A

    2. 17 (22%) had frameshift variants

      PatientID: 46

      KindredID: 46 **

      Case: Sex, Age, Ethnicity unknown

      DiseaseAssertion: VHL

      FamilyInfo: ** Patients 46, 50, 71, and 72 were reported previously in Aronoff et al, 2018 (PMID: 29437867) as family 5

      CasePresentingHPOs: HP:0010797 (hemangioblastoma)

      CaseHPOFreeText: CNS hemangioblamstoma

      CaseNotHPOs: HP:0030421; HP:0009711; HP:0030405; HP:0006770; HP:0100634 (epididymal tumour, retinal capillary hemangioma, pancreatic endocrine tumour, clear cell renal cell carcinoma, neuroendocrine neoplasm)

      CaseNotHPOFreeText: patient was not recorded to have an epididymal tumor, a pancreatic endocrine tumour (pancreatic neuroendocrine neoplasm), CCRCC, nor a neuroendocrine neoplasm (pheochromocytoma/paraganglioma)

      CasePreviousTesting: N/A

      PreviouslyPublished: 29437867

      SupplementalData: Yes; see table S1 for VHL subject genetic and manifestation information.

      Variant: p.F136Lfs*23 (c.408delT)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 43601 https://www.ncbi.nlm.nih.gov/clinvar/variation/43601/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: minus_1_frameshift_variant

      CivicName: F136Lfs*23 (c.408delT)

      MultipleGeneVariants: N/A

    1. PatientID: III-9

      KindredID: 1

      Case: F, 32Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: Large multigenerational family with a history of both VHL and spinocerebellar ataxia type 2 (SCA2). Screening for clinical and genetic diagnostics were gathered as well as thorough information on non-living members. See family pedigree (Fig. 1).

      CasePresentingHPOs: HP:0010797; HP:0009711; HP:0000541; HP:0002542; HP:0001737; HP:0000107; HP:0030405; HP:0001272; HP:0007366; HP:0010873; HP:0001251; HP:0001260; HP:0001310 (hemangioblastoma, Retinal capillar hemangioma, Retinal detachment, Olivopontocerebellar atrophy, Pancreatic cysts, Renal cyst, Pancreatic endocrine tumor, Cerebellar atrophy, Atrophy/Degeneration affecting the brainstem, Cervical spinal cord atrophy, Ataxia, Dysarthria, Dysmetria)

      CaseHPOFreeText: diagnosed with VHL in her early teenage years. She had retinal involvement beginning at the age of 13 treated by cryotherapy and laser therapy (presumably for retinal angiomas); and retinal detachment at the age of 23 requiring eye surgery. She had cysts of the pancreas and kidney detected at 22 years. She has also carried the diagnosis of OPCA since the age of 26-28 (new onset slurred speech and illegible handwriting). Patient had multiple renal cysts without renal tumours, however a large infiltrative enhancing mass in the tail of the pancreas was suggestive of a neuroendocrine/islet cell carcinoma, and liver metastatic foci

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.E160Sfs*10 (c.477delA)

      LegacyVariant: c.688delA

      CaseProblemVariantFreeText: c.477del, p.Glu160Serfs10 should be used. Details: 477del same as 475delA bc that codon is AAA so doesn't matter which A gets deleted: there is an A at 475 476 477 so for HGVS we say that 477 (the latter) is deleted since that follows HGVS nomenclature. Thus use c.477del: p.Glu160Serfs10

      ClinVarID: 182959 https://www.ncbi.nlm.nih.gov/clinvar/variation/182959/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: minus_1_frameshift_variant

      CivicName: E160fs (c.477del)

      MultipleGeneVariants: SCA2 (an abnormal increase in CAG repeats in one allele of her ataxin-2 gene. This abnormal trinucleotide expansion is consistent with the diagnosis of spinocerebellar ataxia type 2)

    1. A 23-yr-old asymptomatic female presented with a palpable mass on the left side of the neck during a routine check-up for her VHL p.Arg64Pro family-specific mutation, already previously identified in this patient’s family. No other clinical manifestations had been detected until then. Somatostatin receptor scintigraphy revealed a hotspot near the left carotid artery, indicating a paraganglioma. No hypertension or increase in catecholamines was observed. The removed 2.5-cm tumor was histopathologically a paraganglioma. At age 33, there was no recurrence, nor did the patient have other tumors. Interestingly, the VHL disease had a heterogeneous presentation in the family, with bilateral pheochromocytomas and clear cell renal carcinoma as the initial presentation in the father. In addition, the patient’s son underwent a unilateral adrenalectomy for pheochromocytoma at the age of 7.

      PatientID: 4

      KindredID: 4

      Case: F, 23Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: The patient had a family specific p.Arg64Pro mutation, and VHL disease had a heterogeneous presentation in the family. The patient’s father initially presented with bilateral pheochromocytomas and clear cell renal carcinoma, and the patient’s son underwent unilateral adrenalectomy for pheochromocytoma at the age of 7.

      CasePresentingHPOs: HP:0002668 (Paraganglioma)

      CaseHPOFreeText: The patient was asymptomatic and presented with a palpable mass on the left side of the neck during a routine check-up. Somatostatin receptor scintigraphy revealed a hotspot near the left carotid artery, which indicated a paraganglioma. The paraganglioma was 2.5cm in size, and histological examination of it post-resection confirmed it was a paraganglioma. The patient did not present with any later tumors, although the length of follow-up is not specified.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.R64P (c.191G>C)

      ClinVarID: 2226, https://www.ncbi.nlm.nih.gov/clinvar/variation/2226/

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName: R64P(c.191G>C)

      MultipleGeneVariants: N/A

    1. PatientID: 136

      KindredID: 51

      Case: M, 25Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: The proband (patient 136) has a mother (patient 137) who presented with a CNS hemangioblastoma at 32, and renal cell carcinoma/ pheochromocytoma at 38. However, no DNA sample was available for his mother's genetic testing.

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

      CaseHPOFreeText: The proband (patient 136) presented with multiple pancreatic cysts/tumors at 21, renal cell carcinoma at 23, and a CNS hemangioblastoma at 25.

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

      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: p.P146Gfs*14 (c.435_436ins)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA2573131810, https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/by_caid?caid=CA2573131810

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: plus_2_frameshift_variant

      CivicName: P146Gfs*14 (c.435_436insGG)

      MultipleGeneVariants: N/A

  2. Oct 2026
    1. Medical files and histopathology reports of patients who had been operated on before were also reviewed.

      PatientID: IV-19

      KindredID: 1

      Case: F, 25Y0M, Iranian

      DiseaseAssertion: assumed VHL

      FamilyInfo: Familial history was positive. See Fig 1. A total of 43 members of the kindred, 24 males and 19 females, aged 2-77 years were reached for evaluation. It is stated in the paper that all affected subjects (13) were positive for the same mutation (c.500G>A). Additionally, gene sequencing revealed that 4 asymptomatic members of the kindred also harbored the pathogenic mutation. Phenotypes include pheochromocytoma, hemangioblastoma, and retinal HB.

      CasePresentingHPOs: HP:0002666; HP:0006880 (Pheochromocytoma, cerebellar hemangiomblastoma)

      CaseHPOFreeText: Patient had a unilateral PCC and cerebellar HB at 23Y which was surgically removed at the time. She presently has no abnormal findings.

      CaseNotHPOs: HP:0000077 (abnormality of the kidney)

      CaseNotHPOFreeText: There was no case of kidney tumors among the kindred.

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      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: 0.000003977, https://gnomad.broadinstitute.org/variant/3-10191507-G-A

      VariantEvidence: N/A

      MutationType: missense_variant; transition

      CivicName: R167Q (c.500G>A)

      MultipleGeneVariants: N/A

    1. PatientID: 288

      KindredID: 113

      Case: M, 24Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: The proband (patient 288) presented with a CNS hemangioblastoma, renal cell carcinoma, and multiple pancreatic cysts/tumors at 23, and a retinal angioma at 24. Their sister (patient 289) presented with a CNS hemangioblastoma, retinal angioma, and renal cell carcinoma at 30.

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

      CaseHPOFreeText: The proband (patient 288) presented with a CNS hemangioblastoma, renal cell carcinoma, and multiple pancreatic cysts/tumors at 23, and a retinal angioma at 24.

      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 3 Deletion (c.464-?_642+?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 3 Deletion

      MultipleGeneVariants: N/A

    1. The propositus underwent bilateral adrenalectomy for bilateral pheochromocytoma at age 23 years. Thereafter she remained well until age 54 years when a small vascular lesion, possibly a spinal hemangioblastoma, was identified by a screening MRI. No other central nervous system abnormalities were detected and her ophthalmologic examination was normal. An abdominal ultrasound scan demonstrated a 2.8-cm cyst in the left kidney. A year later she complained of right leg weakness, and slight weakness was confirmed by physical examination. A repeat MRI scan of the spine demonstrated a tiny, avidly enhancing nodule on the dorsal surface of the spinal cord at C3 with a diffuse area of high signal within the cord at that level, similar in appearance to one year prior

      PatientID: None

      KindredID: Family C

      Case: M, 54Y0M, Ethnicity Unknown

      DiseaseAssertion: Assumed VHL

      FamilyInfo: There was no family history of VHL disease or familial pheochromocytoma. Her parents (mother age 85, father age 79) were asymptomatic and were not available for DNA testing. A 58-year-old maternal half-brother was tested and did not carry the mutation.

      CasePresentingHPOs: HP:0006748, HP:0000107, HP:0009713 (adrenal pheochromocytoma, renal cyst, spinal hemangioblastoma)

      CaseHPOFreeText: The patient had bilateral pheochromocytoma. A small vascular lesion was identified by a screening MRI, which that authors of the papers assumed could possibly a spinal hemangioblastoma,

      CaseNotHPOs: None

      CaseNotHPOFreeText: No other central nervous system abnormalities were detected and her ophthalmologic examination was normal.

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.V84L (c.250G>T)

      LegacyVariant: p.V84L (c.463G>T)

      ClinVar: 2236 https://www.ncbi.nlm.nih.gov/clinvar/variation/2236/

      CAID: CA020170 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.250G%3ET

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: V84L (c.250G>T)

      MultipleGeneVariants: N/A

    1. PMID: 20567917

      PatientID: 1

      KindredID: 1

      Case: F, 24Y0M, Brazilian

      DiseaseAssertion: VHL

      FamilyInfo: VHL type 1 family. No family history of VHL disease. Parents were not available for testing. However, this paper reports that this proband belongs to a different family from that reported by Rocha et al. (PMID: 12624160) as Family 1, with 5 individuals.

      CasePresentingHPOs: HP:0010797; HP:0000107; HP:0001737 (hemangioblastoma; renal cysts; pancreatic cysts)

      CaseHPOFreeText: hemangioblastoma diagnosed at 23Y; and renal and pancreatic cysts at 24Y

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 12624160; 32179488

      SupplementalData: Yes

      Variant: p.F76del (c.226_228delTTC)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: NM_000551.3:c.226_228delTTC automaps to NM_000551.3:c.227_229delTCT due to redundancy

      ClinVarID: N/A

      CAID: CA357012 https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.226_228delTTC

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: inframe_deletion

      CivicName: F76del (c.226_228delTTC)

      MultipleGeneVariants: N/A

    1. frameshift mutations (4/16)

      PatientID: 7

      KindredID: 7

      Case: 23Y0M, Sex Unknown, Argentinian

      DiseaseAssertion: VHL

      FamilyInfo: Thus far, it has not been possible to study the parents or close relatives of this patient.

      CasePresentingHPOs: HP:0009711; HP:0000107 (retinal capillary hemangioma; renal cyst)

      CaseHPOFreeText: Aged 22Y at diagnosis (genetic testing); fulfils type 1 VHL clinical diagnosis. Bilateral retinal hemangioblastomas diagnosed at 22Y, and renal cysts were diagnosed at 23Y (See Table 1 & 2).

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.Q132Hfs*45 (c.343_395dup)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA2497030272 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/by_caid?caid=CA2497030272

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: plus_2_frameshift_variant; duplication

      CivicName: Q132Hfs*45 (c.343_395dup)

      MultipleGeneVariants: N/A

    1. A 33-year-old man was admitted to Zhongda Hospital, Southeast University (Nanjing, China) with a two-month history of progressive right flank pain, accompanied by a one-month history of recurrent painless gross hematuria. The patient's previous medical history included urological surgery at the age of 23 years due to an epididymal cyst and an ophthalmologic surgery at 26 years of age for retinal detachment resulting from bilateral retinal angiomatosis, which was performed at Shuyang People's Hospital (Suqian, China). At the time of the present study, the patient had two children, a son and a daughter, who were in good health; his father, aged 65 years, and his mother, aged 62 years, were also in good health. The patient's two brothers, aged 40 and 37 years old, with one child each were all are in good health.

      PatientID: N/A

      KindredID: 1

      Case: M, 33Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: Genetic analysis of the patient's parents and brothers, who were unaffected, confirmed a diagnosis of de novo VHL disease.

      CasePresentingHPOs: HP:0030424, HP:0009711, HP:0005584, HP:0006770, HP:0001737, HP:0000107 (epididymal cyst, retinal capillary hemangioma, renal cell carcinoma, clear cell renal cell carcinoma, pancreatic cysts, renal cyst)

      CaseHPOFreeText: He was admitted to the hospital with a two-month history of progressive right flank pain, accompanied by a one-month history of recurrent painless gross hematuria. The patient's previous medical history included urological surgery at the age of 23 years due to an epididymal cyst and an ophthalmologic surgery at 26 years of age for retinal detachment resulting from bilateral retinal angiomatosis. Contrast-enhanced computed tomography (CT) scanning and angiography were used to detect the presence of quasi-circular enhancing lesions in the middle of the left kidney and large irregular enhancing lesions in the right kidney, extending into the vena cava, that formed an embolus. In addition, multiple cysts in the pancreas and kidney were detected radiologically. The patient underwent a radical nephrectomy with an embolectomy of the right kidney for treatment of T3b-stage renal cell carcinoma. After three months, he successfully underwent laparoscopic nephron-sparing surgery (NSS) of the left kidney. Histological analysis of the renal tissue revealed clear cell carcinomas.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.S65W(c.194C>G)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 43597 https://www.ncbi.nlm.nih.gov/clinvar/variation/43597/

      CAID: CA020099 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.194C%3EG

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName:S65W(c.194C>G)

      MultipleGeneVariants: N/A

    1. PatientID: 8

      KindredID: 5

      Case: M, 5Y0M, Ethnicity Unknown

      DiseaseAssertion: Asymptomatic

      FamilyInfo: Positive. The patient's mother (5) and aunt (4) were confirmed to have the mutation and had VHL presentations. The patient's cousin was the proband (1) and also had the mutation and presented with hemangioblastoma and abnormality of the pancreas.The grandfather (13) was inferred to have the mutation and had a hemangioblastoma. See Figure 2a for family pedigree.

      CohortInfo: 20 unrelated VHL families from an ethnically diverse cohort containing both affected and unaffected individuals.

      CasePresentingHPOs: N/A

      CaseHPOFreeText: N/A

      CaseNotHPOs: HP:0009711, HP:0005584, HP:0002666, HP:0001732, HP:0000077, HP:0010797 (retinal capillary hemangioma, renal cell carcinoma, pheochromocytoma, abnormality of the pancreas, abnormality of the kidney, hemangioblastoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 31368132

      SupplementalData: Supplementary file 1.

      Variant: p.F136Lfs*23 (c.408delT)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 43601 https://www.ncbi.nlm.nih.gov/clinvar/variation/43601/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: minus_1_frameshift_variant

      CivicName: F136Lfs*23 (c.408delT)

      MultipleGeneVariants: N/A

    2. Proband presented at 10 years of age with a cerebellar haemangioblastoma and pancreatic lesions, detected by symptom. She was subsequently found to carry a c.408delT pathogenic variant of the VHL gene.

      PatientID: 1

      KindredID: 5

      Case: F, 13Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: Positive. The patient's mother (4) also carried this mutation and had a hemangioblastoma. The proband's aunt (5) was confirmed to have the mutation and had VHL presentations. The cousin (8) had the mutation but was asymptomatic. The grandfather (13) was inferred to have the mutation and had a hemangioblastoma. See Figure 2a for family pedigree.

      CohortInfo: 20 unrelated VHL families from an ethnically diverse cohort containing both affected and unaffected individuals.

      CasePresentingHPOs: HP:0010797, HP:0001732 (hemangioblastoma, abnormality of the pancreas)

      CaseHPOFreeText: The patient presented with a hemangioblastoma and abnormality of the pancreas at age 10.

      CaseNotHPOs: HP:0009711, HP:0005584, HP:0002666, HP:0000077 (retinal capillary hemangioma, renal cell carcinoma, pheochromocytoma, abnormality of the kidney)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 31368132

      SupplementalData: Supplementary file 1.

      Variant: p.F136Lfs*23 (c.408delT)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 43601 https://www.ncbi.nlm.nih.gov/clinvar/variation/43601/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: minus_1_frameshift_variant

      CivicName: F136Lfs*23 (c.408delT)

      MultipleGeneVariants: N/A

    3. PatientID: 16 (Uncle)

      KindredID: 18

      Case: M, 68Y0M, Ethnicity Unknown

      DiseaseAssertion: Assumed VHL

      FamilyInfo: 11 members of this family tested positive for the c.712C>T/c.499C>T germline variant of the VHL gene. 14 members of this family were assumed to carry this variant due to family history/personal medical history. Members of this family range from asymptomatic to multi-organ involvement (pheochromocytoma, pancreatic and renal cysts/tumors and hemangioblastomas). The family was previously reported in PMID 3942913.

      CasePresentingHPOs: HP:0002666; HP:0005584; HP:0010797 (Pheochromocytoma, Renal cell carcinoma, Hemangioblastoma)

      CaseHPOFreeText: This patient presented with pheochromocytoma (23Y). Age of diagnosis for CNS hemangioblastoma and renal cell carcinoma is unknown.

      CaseNotHPOs: HP:0000077; HP:0001732; HP:0009711 (Abnormality of the kidney, Abnormality of the pancreas, Retinal capillary hemangioma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 3942913 (some members of this family are previously reported (phenotypes only) but unable to match patients across papers with confidence)

      SupplementalData: Supplementary Table 1.

      Variant: N/A

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Authors state that the c.712C>T germline familial variant of the VHL gene in this patient is “inferred from the family”. No genetic testing was done on this patient to confirm this. Being that this familial variant is out of bound with respect to the NM_000551.3 reference sequence, it was concluded that this variant is noted in the Latif et al. (1993) reference and was translated to c.499C>T (NM_000551.3).

      MutationType: N/A

      CivicName: N/A

      MultipleGeneVariants: N/A

    1. c.269A > T p.Asn90Ile (group 8)

      GroupID: 8

      DiseaseAssertion: assumed VHL

      GroupSize: 15

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: Chinese

      GroupAgeRange: 36.9Y +/- 15.6Y

      GroupInfo: Clinical characteristics of 258 patients from 80 unrelated Chinese families were reported in this study. Grouped by the 21 mutations found, 3 families with 15 members total were described, and phenotypic information was given for this group.

      GroupPresentingHPOs: HP:0010797; HP:0009711; HP:0005584; HP:0001737; HP:0002666 (hemangioblastoma, retinal capillary hemangioma, renal cell carcinoma, pancreatic cysts, pheochromocytoma)

      GroupHPOFreeText: 10 of the 15 members presented with CNS hemangioblastoma (mean age of 29.9Y), 2/15 had retinal capillary hemangiomas at 23Y and 30Y, renal cell carcinoma in 4 members (at a mean age of 41.5Y), pancreatic cysts in 5 members (with a mean age of onset of 41.4Y), and 1 member with pheochromocytoma at 38Y

      GroupNotHPOs: HP:0009715 (papillary cystadenoma of the epididymis)

      GroupNotHPOFreeText: No patients were given with papillary cystadenoma of the epididymis

      GroupPreviousTesting: N/A

      PreviouslyPublished: 29330336; 28388566

      SupplementalData: N/A

      Variant: p.N90I (c.269A>T)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 223172 https://www.ncbi.nlm.nih.gov/clinvar/variation/223172/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: N90I (c.269A>T)

      MultipleGeneVariants: N/A

    1. IV/13 (27)-+ (22)-+ (23)renal cysts (20)Ser80Ile

      PatientID: IV-13

      KindredID: 1

      Case: F, 27Y0M, Hungarian

      DiseaseAssertion: VHL

      FamilyInfo: The patient had an affected brother (IV-14) who carried the Ser80Asn mutation and presented with pheochromocytoma and retina hemangioblastoma. The patient's mother (III-7) carried the same mutation and had a brain hemangioblastoma and retina hemangioblastoma. The uncle (III-8) harboured the same mutation and had brain hemangioblastoma, pheochromocytoma, and retina hemangioblastoma. He had three kids, out of which only one carried the mutation but was asymptomatic (IV-16). The patient's grandmother (II-5) also harboured the same mutation and presented with renal cell carcinoma. This patient's great aunt (II-1) carried two different VHL mutations; the Ser80Asn and Pro25Leu but herself was asymptomatic. She passed the Ser80Asn mutation to her daughter, the proband (III-1), who had renal cell carcinoma, brain hemangioblastoma, and pheochromocytoma. Refer to figure 1 for pedigree.

      CasePresentingHPOs: HP:0010797, HP:0009711, HP:0000107 (hemangioblastoma, retinal capillary hemangioma, renal cyst)

      CaseHPOFreeText: The patient presented with brain hemangioblastoma at age 22, retina hemangioblastoma at age 23, and renal cysts at age 20.

      CaseNotHPOs: HP:0005584, HP:0002666 (renal cell carcinoma, pheochromocytoma )

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.S80N (c.239G>A)

      LegacyVariant: p.S80I (c.239G>A) *author mistake

      CaseProblemVariantFreeText: N/A

      ClinVarID:N/A

      CAID: CA70046108 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.239G%3EA

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: S80N (c.239G>A)

      MultipleGeneVariants: N/A

    1. GroupID: 15

      Case: 23Y0M, Sex Unknown, Ethnicity Unknown

      DiseaseAssertion: assumed VHL

      FamilyInfo: 1 of the 573 patients discussed in this paper were found to have this variant. This mutation was found in 1 VHL family with a single patient.

      CasePresentingHPOs: HP:0009711; HP:0006880 (retinal capillary hemangioma; cerebellar hemangioblastoma)

      CaseHPOFreeText: patient had retinal angiomas at 21Y and cerebellar hemangioblastomas diagnosed at 23Y

      CaseNotHPOs: HP:0005584; HP:0002666 (renal cell carcinoma; pheochromocytoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplementary Table S1.

      Variant: p.F91* (c.272_273delinsAA)

      CaseProblemVariantFreeText: c.272T>A and c.273C>A results in c.272_273delinsAA

      LegacyVariant: N/A

      ClinVarID: CA2499307077 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/by_caid?caid=CA2499307077

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: delins; stop_gained

      CivicName: F91* (c.272_273delinsAA)

      MultipleGeneVariants: N/A

    1. IV - 10

      PatientID: IV:10

      KindredID: 1

      Case: F, 28Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: A 5-generation family with VHL in 15 members. Both second generation children (presumed), 5 third generation, and 8 further generation individuals were affected and haplotyping was conducted using three polymorphic microsatellite markers. All of the 5th generation children (9 total at time of publication) had been sequenced and haplotyped as unaffected.

      CasePresentingHPOs: HP:0006880; HP:0000107 (cerebellar hemangioblastoma, renal cysts)

      CaseHPOFreeText: patient had cerebellar HB; renal cysts. Age of onset was 23Y, and surgery (operation) was 28Y

      CaseNotHPOs: HP:0002666; HP:0030405; HP:0001737; HP:0002668 (pheochromocytoma, pancreatic endocrine tumor, pancreatic cysts, paraganglioma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

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

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

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

      CAID: N/A

      gnomAD: 0.000007954, https://gnomad.broadinstitute.org/variant/3-10191506-C-T?dataset=gnomad_r2_1

      VariantEvidence: genotyped three polymorphic microsatellite markers that flanked VHL on chromosome 3p25 (D3S3691, D3S1597 and D3S1263). 

      MutationType: missense_variant;transition

      CivicName: R167W (c.499C>T)

      MultipleGeneVariants: N/A

  3. Mar 2026
  4. Dec 2025
    1. There was one thing to be done before I left, an awkward, unpleasant thing that perhaps had better have been let alone. But I wanted to leave things in order and not just trust that obliging and indifferent sea to sweep my refuse away. I saw Jordan Baker and talked over and around what had happened to us together, and what had happened afterward to me, and she lay perfectly still, listening, in a big chair. She was dressed to play golf, and I remember thinking she looked like a good illustration, her chin raised a little jauntily, her hair the colour of an autumn leaf, her face the same brown tint as the fingerless glove on her knee. When I had finished she told me without comment that she was engaged to another man. I doubted that, though there were several she could have married at a nod of her head, but I pretended to be surprised. For just a minute I wondered if I wasn’t making a mistake, then I thought it all over again quickly and got up to say goodbye.

      wow the breakup trauma,they didn't end well

    2. om,” I inquired, “what did you say to Wilson that afternoon?” He stared at me without a word, and I knew I had guessed right about those missing hours. I started to turn away, but he took a step after me and grabbed my arm. “I told him the truth,” he said. “He came to the door while we were getting ready to leave, and when I sent down word that we weren’t in he tried to force his way upstairs. He was crazy enough to kill me if I hadn’t told him who owned the car. His hand was on a revolver in his pocket every minute he was in the house—” He broke off defiantly. “What if I did tell him? That fellow had it coming to him. He threw dust into your eyes just like he did in Daisy’s, but he was a tough one. He ran over Myrtle like you’d run over a dog and never even stopped his car.”

      wow,tom told the truth to george,poor guy,but george doesn't seem to accept the truth

    3. He murdered her.” “It was an accident, George.” Wilson shook his head. His eyes narrowed and his mouth widened slightly with the ghost of a superior “Hm!” “I know,” he said definitely. “I’m one of these trusting fellas and I don’t think any harm to nobody, but when I get to know a thing I know it. It was the man in that car. She ran out to speak to him and he wouldn’t stop.” Michaelis had seen this too, but it hadn’t occurred to him that there was any special significance in it. He believed that Mrs. Wilson had been running away from her husband, rather than trying to stop any particular car.

      george start to accuse gastby as the murderer of his wife,i think hisa poor guy,everyone has been hiding secret from him.

    4. I wanted to get somebody for him. I wanted to go into the room where he lay and reassure him: “I’ll get somebody for you, Gatsby. Don’t worry. Just trust me and I’ll get somebody for you—”

      Nick cares about Gatsby. He wants to make sure he is not alone. It also shows how abandoned Gatsby is at the end.

    5. After the armistice he tried frantically to get home, but some complication or misunderstanding sent him to Oxford instead. He was worried now—there was a quality of nervous despair in Daisy’s letters. She didn’t see why he couldn’t come. She was feeling the pressure of the world outside, and she wanted to see him and feel his presence beside her and be reassured that she was doing the right thing after all.

      Daisy’s decision was shaped by fear and pressure than by a lack of love. She need reassurance and stability, but Gatsby couldn’t give her at the time, this is the reason why she turned to Tom.

  5. Oct 2025
    1. My br other is also a physician, and also of high standing,and he says the same thing.

      It’s interesting that either her husband or her brother are all physician and had same idea about her. It shows that how stressful the narrator would be if none of them believed she was sick.

  6. Sep 2025
    1. I don’t like our room a bit. I wanted one downstairs thatopened on the piazza and had roses all over the window, andsuch pretty, old-fashioned chintz hangings! but John wouldnot hear of it.He said there was only one window and not room for twobeds, and no near room for him if he took an other.He is very careful and loving, and hardly lets me stir withoutspecial direction

      This passage is troubling to me. John calls himself loving, but he controls every part of her life.This didn’t make her condition better,but made it worse.

    2. John is a physician, and perhaps— (I would not say it to a livingsoul, of course, but this is dead paper and a great relief to mymind)— perhaps that is one reason I do not get well faster

      I find this interesting because it shows irony. The narrator’s husband is a doctor, but instead of helping her recover, his actually makes her worse.

    3. I’ve got out at last,” said I, “in spite of you and Jane! AndI’ve pulled off most of the paper, so you can’t put me back!”

      This is troubling because the narrator believes she has escaped by tearing down the wallpaper, but in reality she has lost her sanity.

    4. That spoils my ghostliness, I am afraid; but I don’t care—there is something strange about the house— Ican feel it.

      The narrator sensed something that makes her insecure and afraid. And her emotions got triggered unreasonably because of it.

    5. Personally I believe that congenial work, with excitement andchange, would do me good.

      His husband and brother are both physicians, but they don’t seem to understand psychiatry. I actually think the main character, as a mental patient, knows better how to heal herself.

    6. Now why should that man have fainted?

      Surprising: This sentence surprising me because narrator have no idea what she done is crazy, she even confuse about why her husband fainted, showing she completely lose her mind.

  7. Aug 2025
    1. https://sustainingcommunity.wordpress.com/2019/02/01/4-types-of-power/#comment-122967

      Given your area, if you haven't found it yet, you might appreciate going a generation further back in your references with: Mary P. Follett. Dynamic Administration: The Collected Papers of Mary Parker Follett, ed. by E. M. Fox and L. Urwick (London: Pitman Publishing, 1940). She had some interesting work in organization theory you might appreciate. Wikipedia can give you a quick overview. https://en.wikipedia.org/wiki/Mary_Parker_Follett#Organizational_theory

  8. May 2025
    1. Drei führende Klimawissenschaftler kritisieren die Illusion der "Net Zero-Politiken", die darauf setzen, das 1,5°-Ziel durch die Entfernung von CO2 aus der Atmosphäre zu erreichen. Sie werfen vielen ihrer KollegInnen vor, unrealistischen Konzepten nicht offen entgegenzutreten, um ihren politischen Einfluss nicht zu verlieren. Sie kritisieren auch die bisherigen Integrated Assessment Models des Weltklimarats, die von der Voraussetzung ausgehen würde, die Klimakatastrophe ließe sich mit marktwirtschaftlichen Mitteln beheben und fordern auf, deutlich zu sagen, dass sich eine Erhitzung der Erde auf 3 und mehr Grad nicht durch kleine Schritte, sondern nur durch einen Bruch mit dem bisherigen Wirtschaftssystem erreichen lässt.

      Anstatt uns unseren Zweifeln zu stellen, beschlossen wir Wissenschaftler, immer aufwändigere Fantasiewelten zu konstruieren, in denen wir sicher wären. Der Preis, den wir für unsere Feigheit zahlen mussten: Wir mussten den Mund halten über die immer größer werdende Absurdität der geforderten Kohlendioxid-Entfernung im planetarischen Maßstab.

      Greta Thunberg hat diesen Aufsatz als einen wichtigsten und informativsten Texte zur Klima- und ökologischen Krise bezeichnet.

      Climate scientists: concept of net zero is a dangerous trap. Thread von Greta dazu auf Twitter: https://twitter.com/GretaThunberg/status/1385869663188492290

  9. Apr 2025
    1. Bei einem virtuellen Gipfel der Vereinten Nationen zur Klimakrise haben sich Hina, D.E.U., D.A. sehr anstatten die afrikanische Union Brasilien und die Koalition der kleinen Inselstaden zur Energiewände und einer Internationalen Klamot-Gavernans bekannt. Der chinesische Staatschef Schie, der was selten ist, an dem Treffen teilnahmen, verwies darauf, dass China die inzwischen größte Infrastruktur für erneuerbare Energie entwickelt hat, einschließlich der dazu gehörrenden Liefer. Einst du sie sich dazu gehörenden Lieferketten. Die Teilnehmer starten werden ihre nationalen Reduktionsstrategien rechtzeitig vor der Kopf 30 erstellen. https://www.theguardian.com/environment/2025/apr/23/un-chief-no-group-or-government-can-stop-clean-energy-future

    1. Der neue Planetary Health Check des Potsdam Instituts für Klimafolgenforschung ergibt, dass durch die Versauerung der Ozeane möglicherweise gerade die siebte von 9 planetaren Grenzen durchbrochen wird und die Biosphäre auch hier in eine Hochrisikozone eintritt. Bei allen anderen mit Ausnahme des Ozonschwunds haben sich die Bedingungen verschlechtert. Die CO2- Emissionen treiben die Versauerung an, die wiederum die Fähigkeit der Ozeane mindert, als CO2-Senke zu wirken. https://www.theguardian.com/environment/2024/sep/23/earth-breach-planetary-boundaries-health-check-oceans

      Website zum Planetary Health Check: https://www.planetaryhealthcheck.org/

    1. The name of the covered recipient.‘‘(ii) The business address of the covered recipientand, in the case of a covered recipient who is a physi-cian, the specialty and National Provider Identifierof the covered recipient.‘‘(iii) The amount of the payment or other transferof value.‘‘(iv) The dates on which the payment or othertransfer of value was provided to the covered recipient.‘‘(v) A description of the form of the payment orother transfer of value, indicated (as appropriate forall that apply) as—‘‘(I) cash or a cash equivalent;‘‘(II) in-kind items or services;‘‘(III) stock, a stock option, or any other owner-ship interest, dividend, profit, or other return oninvestment; or‘‘(IV) any other form of payment

      This is the requirement in the Sunshine Act that reports of payments that physicians have recieved will not include the NPI of the Physician.

  10. Mar 2025
  11. southtexascollege.blackboard.com southtexascollege.blackboard.com
    1. Yet thou triumph’st, and say'st that thou <br /> Find’st not thy self, nor me the weaker now;

      In lines 23 and 24, the listener finally speaks, claiming that by killing the flea, she is not weak. By saying this, she essentially says that there was no harm in killing the flea, as it took both their blood.

  12. Feb 2025
  13. Jan 2025
    1. I think the book is fantastic I'm now going to outlined review of a book and then at the end briefly point out some potential implications for psychiatric diagnosis and neurodiversity

      for - implications of book "The Brain Abstracted" for neurodiversity - SOURCE - Youtube - book review - Reviewing "The Brain Abstracted - Simplification in the History and Philosophy of Neuroscience" - M. Chirimuuta - Youtube channel: Philosophy of Psychiatric Diagnoses - 2025 Jan 23

  14. Dec 2024
    1. Over a 10-year period, up until three weeks before his death, we exchanged 150 letters. After Oliver passed away, I had to find a way to handle my sadness. So, I revisited all our letters and wrote a new book, Dear Oliver: An Unexpected Friendship with Oliver Sacks, as a tribute to exploration, letter-writing, friendship, and Oliver Sacks.

      for - book - Dear Oliver: An Unexpected Friendship with Oliver Sacks - from Psychology Today website - article - What Oliver Sacks Taught Me - Susan R. Barry - 2024 - Jan. 23 - to

      to - book - Dear Oliver: An Unexpected Friendship with Oliver Sacks - Susan R. Barry - 2024, Jan 30 - https://hyp.is/6ir6jME9Ee-vLEu_PiRFsw/theexperimentpublishing.com/catalogs/winter-2024/dear-oliver/

    2. once I began to see in 3D, I realized how wrong I had been. My theoretical knowledge of stereopsis did not prepare me in the least for the experience of seeing in stereo. Dr. Sacks must have suspected that stereopsis would provide me with an astonishing new way of seeing, one that I could not even have imagined

      for - cliche - the finger pointing to the moon - the finger is not the moon - language is NOT the experience it describes - from Psychology Today website - article - What Oliver Sacks Taught Me - Susan R. Barry - 2024 - Jan. 23

    3. I answered Dr. Sacks’s question casually, saying that I believed that I knew what it was like to see in 3D. After all, I was a neurobiology professor and had read plenty of scientific papers on stereopsis.

      for - association - person with 2D vision - trying to imagine what it's like to see in 3D - What's it like to be a bat? - from Psychology Today website - article - What Oliver Sacks Taught Me - Susan R. Barry - 2024 - Jan. 23 - adjacency - seeing in 2D - then in 3D - Deep Humanity BEing journey - from Psychology Today website - article - What Oliver Sacks Taught Me - Susan R. Barry - 2024 - Jan. 23

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