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    Human GBP4 promotes TRIM21-BIP-dependent autophagy to restrict M. tuberculosis infection by preventing SORT1-mediated progranulin degradation
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    sciencedirect.com/science/article/pii/S221112472600817X
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    Vascular signals coordinate cerebellar circuitry development
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    Tracing NAD+ metabolism uncovers adaptive coordination between host and microbiome during colitis
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    Distributed clonal deletion prevents autoimmune disease progression
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    Sex differences in somatosensory circuitry are programmed by developmental microglia-astrocyte interaction
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    Dynamic dimer-of-dimers architecture defines Mg2+ transport in human CNNM4
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    A Remove-Remodel-Repair Strategy Enabled by a Spatiotemporally Controlled Hydrogel for Integrative Osteosarcoma Therapy
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    Lactate Promotes Macrophage-Derived Foam Cell Formation and Atherosclerosis
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    RNA exonuclease REXO4 resolves m6A-marked R-loops and suppresses anti-tumor immunity
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    A bivalent molecular glue linking lysine acetyltransferases to oncogene-induced cell death
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    In vivo models of subclonal oncogenesis and dependency in hematopoietic malignancy
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  15. Local file Local file
    Pen, Ink, Keys, and Cards: Some Reflections on Library Technology
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    5. chrisaldrich 27 Jul 2026
      Other ideas,such as the electric pen, looked promis-ing, at least at first, judging from com-ments in the library press in 1877 and1879. The pen's story proves that inven-tions must not only serve a general need,they must adapt to the specific require-ments of libraries and conform withother existing technologies. Invented byThomas Alva Edison and patented in1876, the electric pen was a writing in-strument that used electromagnets and asmall storage battery. The actual pen,connected by wire to the power source,resembled a sewing needle; it producedsmall punctures in the form of letters andnumbers, and when an inked roller waspassed over the resulting stencil plate,legible copies could be made.
      electric pen Thomas A. Edison inventions technology copying duplicator machines
    6. chrisaldrich 27 Jul 2026
      We maychuckle at John Cotton Dana's proposalin 1907 to use vending machines, justcoming into popular use for chewinggum and novelties, to display and circu-late books, but the concept behind themachine-that of the self-service li-brary-was and is a good idea. In hissuggestion that users insert their librarycard (or more precisely an encodedmetal strip "not larger than a Yale key")so borrower data could be recorded, wesee a distinctly modern application oftechnology to solve a library problem.

      I've actually used a library vending machine that had books and DVDs in it in the last 2 years at a local pizza parlor.

      vending machines libraries John Cotton Dana 1907 book circulation library cards

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    Discards
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    1. chrisaldrich 27 Jul 2026

      Baker, Nicholson. 1994. “Discards.” The New Yorker 70(7): 64. https://www.newyorker.com/magazine/1994/04/04/discards (August 6, 2021).

      library card catalog Rolodexes collocation digitization card index as database Fred Kilgour Online Computer Library Center (OCLC) authority control French Cataloging Code of 1791 MARC (Machine-Readable Cataloging) References read art Harvard University Widener Libraray Tom Johnston Maureen Finn Vladimir Nabokov Timofey Pnin Judith Brugger Velveteen Rabbit subject searching New York Public Library Virginia Pratt
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    Induced pluripotent stem cell line BIOi003-A from a patient with ABCA4-associated retinal dystrophy carrying compound heterozygous c.(1222C>T;2919-884G>T) variants in ABCA4
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  18. pubmed.ncbi.nlm.nih.gov pubmed.ncbi.nlm.nih.gov
    Application of targeted exome and whole-exome sequencing for Chinese families with Stargardt disease
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  19. iovs.arvojournals.org iovs.arvojournals.org
    Mutations in ABCR (ABCA4) in Patients with Stargardt Macular Degeneration or Cone-Rod Degeneration
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  20. www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov
    Exome Sequencing of 47 Chinese Families with Cone-Rod Dystrophy: Mutations in 25 Known Causative Genes
    1
    1. Vibhor 27 Jul 2026
      Family 1ABCA4c.[1957C>T];[4604dup]M7.06.0PV, PP0.200.15MA, TPOD, ARAMA, TPOD, ARANormalReduced

      Case#: Family 1 proband, male, 6yo at onset, Chinese

      DiseaseAssertion: CORD

      FamilyInfo: heterozygous unaffected parents

      CasePresentingHPOs: HP:0000613, HP:0000505, HP:0007401, HP:0012511, HP:0008043, HP:0000512

      CaseHPOFreeText:  ERG responses from cones reduced, BVA=0.20/0.15

      CaseNotHPOs:

      CaseNotHPOFreeText:

      PreviouslyPublished: n/a

      Variant: c.[1957C>T];[4604dup] phase confirmed

      ClinVar: n/a

      CAID: CA645372205

      SupplementalData:

      CA645372205 CaseInfo Individual automated_hgnc:34 automated_hgnc_source:CAID ClinGen ABCA4 Annotations
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    ncbi.nlm.nih.gov/pmc/articles/PMC3679152/
  21. onlinelibrary.wiley.com onlinelibrary.wiley.com
    Fine central macular dots associated with childhood-onset Stargardt Disease
    1
    1. Vibhor 27 Jul 2026
      two siblings were from one consanguineous family (case 1, 11 years and case 2, 9 years)

      Case#: two siblings (female) were from one consanguineous family (case 1, 11 years and case 2, 9 years)

      DiseaseAssertion: Stargardt’s Disease

      FamilyInfo: NR

      ParentalTesting: NR

      CasePresentingHPOs: HP:0030500, HP:0011507

      CasePhenotypeFreeText: LogMAR visual acuity for the right and left eye of cases 1–4 was 0.3 and 0.2, 0.1 and 0.1, 0.5 and 0.4, and 0.3 and 0.4, respectively. Gross disruption of the outer retinal layers at the macula in all cases; in two (cases 2 and 4), the presumed external limiting membrane (ELM) peak was broadened with the inner segment ellipsoid band (ISe) missing. Subtle white-yellowish fine dots at the macula and numerous white-yellowish flecks extending anterior to the arcade are shown in the colour fundus photograph of case 1. Autofluorescence (AF) imaging of case 1 detected well-defined dots with high signal at the central macula surrounded by a ring of increased signal and numerous foci with high or low signal extending to the peripheral retina. Case 2 also had subtle white-yellowish fine dots at the central macula and numerous white-yellowish flecks extending anterior to the arcade, both associated with high signal on AF imaging. In addition, case 3 had white-yellowish fine dots at the macula and numerous white-yellowish flecks extending to the periphery, both of which had high or low signal on AF imaging. Case 4 showed subtle fine macular dots mainly in a para-foveal location, which are well-defined on AF imaging.

      CaseNotHPOs: HP:0007401, HP:0000505

      CaseNotPhenotypeFreeText: Most cases with STGD have central macular atrophy with numerous more peripheral flecks (Michaelides et al. 2003). Given their relatively good visual acuity, it is likely that the central macular dots observed in our cases may be an early sign of macular dysfunction before the development of macular atrophy. Similar fine macular dots or a ‘mottled macula’ have also been reported in other inherited retinal diseases

      CasePreviousTesting: The age of disease onset in cases 1–4, defined as either the age at which visual loss was first noted by the subject or in the asymptomatic subjects when abnormal retinal appearance was first detected, was 5, 7, 8, and 6 years old, respectively.

      GenotypingMethod: After informed consent was obtained, blood samples were taken from probands of 2/3 families for ABCA4 screening. A full medical history was obtained, and a full ophthalmologic examination was performed in all cases. Mutation screening of ABCA4 was performed in two probands of the three families, and two likely disease-causing variants were identified in each case; c.768G > T, p.V256V (a previously reported splicing-altering synonymous variant) and c.4363T > C, p.C1455R (a missense variant) in case 1, and c.1906C > T, p.Q636* (a non-sense variant) and c.5461-10 T > C (a disease-associated intronic variant with uncertain effect) in case 3. A blood sample was not available in one proband (case 4).

      Variant: NM_000350.3(ABCA4):c.768G>T (p.Val256=) and NM_000350.3(ABCA4):c.4363T>C (p.Cys1455Arg)

      LegacyVariant: c.768G>T (p.Val256=) and c.4363T>C (p.Cys1455Arg)

      ClinVar: 99505 and 377404

      CAID: CA227458 and CA957621

      gnomeAD: 1:94564350 C / A and 1:94495177 A / G

      MultipleGeneVariants:No

      PreviouslyPublished: No

      AdditionalInfo: Some symptoms/diagnoses are consistent with Stargardt’s Disease 3, however the probands in the study were younger in age, so many of the symptoms hadn’t progressed much. Also, all of the cases had decent visual acuity, which contradicts a symptom of Stargardt’s Disease 3.

      InheritancePattern:NoInheritanceAssertion DiseaseAssertion:Starghardt'sDisease Mutation:Missense Zygosity:Heterozygous Clinvar:377404 CAID:CA957621 PreviousTesting automated_hgnc:34 automated_hgnc_source:CAID ClinGen ABCA4 Annotations
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    onlinelibrary.wiley.com/doi/10.1111/aos.12259
  22. www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov
    Protein misfolding and the pathogenesis of ABCA4-associated retinal degenerations
    1
    1. Vibhor 27 Jul 2026
      both the P and PV ABCA4 variants exhibited a dramatically reduced basal ATPase activity (∼30% of WT ABCA4), which did not increase upon the addition of all-trans-retinal. Thus, ABCA4 variants carrying the P mutation were functionally impaired.

      ATPase activity in HEK293 cells showed severely reduced basal ATPase activity, ∼30% of WT ABCA4, indicating that this variant impacts protein function (PS3_Supporting; PMIDs).

      PS3 CA226911 automated_hgnc:34 automated_hgnc_source:CAID ClinGen ABCA4 Annotations
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    ncbi.nlm.nih.gov/pmc/articles/PMC4424957/
  23. pmc.ncbi.nlm.nih.gov pmc.ncbi.nlm.nih.gov
    High-Throughput Sequencing to Identify Mutations Associated with Retinal Dystrophies
    1
    1. Vibhor 27 Jul 2026
      024 m Caucasian STGD ABCA4 NM_000350.2 c.[6601_6602delAG];[=], c.[4253+43G>A];[=] p.Arg2201fs* p.Ile1377Hisfs*3 Not found 0.004694 AR Pathogenic Pathogenic 2 [36] [19]

      Case#: Patient 24, male, Caucasian, onset at 50yo, Germany

      DiseaseAssertion: STGD

      FamilyInfo: co-segregation of variant in 2 family members (siblings) but they do not appear to be affected based on pedigree

      CasePresentingHPOs: HP:0030528, HP:0000505, HP:0012508, HP:0001105, HP:0025148

      CaseHPOFreeText: progressive paracentral scotoma OU, progressive visual impairment OU (blurry vision). BCVA: OD-0.1, OS-0.22. Tension: 13mmHg/14mmHg. FAF: bilateral hyperautofluorescent macular and peripapillary spots, few spots of paracentral retinal atrophy (foveal sparing). Autofluorescence and deposits (severity): deposits medium, atrophy low. OCT: hyperreflective spots, partially invading into the outer retina, partly confluent lesions of cRORA, foveal sparing, degenerative intraretinal fluid. Central macular thickness: 328µm/322µm. Macular volume: 9.31mm³/9.00mm³. mfERG: bilateral amplitudes in normal range, slight relative reduction in the paracentral areas. Fluorescein angiography: bilateral dark choroid, mild paracentral dye pooling in the late phase. Color vision: Inconspicuous. Clinical examination: pattern-like distribution of the lesions.

      CaseNotHPOs: n/a

      CaseNotHPOFreeText: n/a

      GenotypingMethod: WES, in-house RD-associated gene panel including 619 candidates and disease-associated genes

      PreviouslyPublished: n/a

      Variant: ABCA4 NM_000350.2 c.[6601_6602delAG] (p.Arg2201fs);[=], c.[4253+43G>A] p.Ile1377Hisfs3;[=]

      CAID: CA227421; CA227172

      SupplementalData: phenotype and segregation info in supplemental data (table s1, figure s1)

      CAID:CA227421 CaseInfo Individual CAID:CA227172 Scotoma DecreasedCentralVA FundusAutofluorescence DiseaseEntity:STGD1 InheritancePattern:AutosomalRecessive Zygosity:CompoundHeterozygous SupplementalData automated_hgnc:34 automated_hgnc_source:CAID ClinGen ABCA4 Annotations
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    pmc.ncbi.nlm.nih.gov/articles/PMC8391535/