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    PADI-dependent mitochondrial adaptation drives resistance to KRAS inhibitors
    34
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    The left PBN to aCM pathway mediates pain-related aversion in male mice
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    Skin commensals shape the clock-ferroptosis axis to preserve barrier function in psoriasis
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    Albumin uptake through FcRn promotes tumor-associated macrophage maturation and albumin-bound immunotherapy response
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    Engineering a Model Cell for Rational Tuning of GPCR Signaling
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    Myeloid reprogramming generates myeloid-derived activating cells to potentiate radiotherapy and suppress metastasis
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    Apelin Receptor Signaling Protects GT1-7 GnRH Neurons Against Oxidative Stress In Vitro
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    CuO Quantum Dots@amorphous CoOOH Semiconductor Heterostructure for Label-Free Surface-Enhanced Raman Scattering Detection and Accurate Classification of Gastrointestinal Tumor Cells
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    A Post–NGP <i>Mitsuokella jalaludinii</i> as a Therapeutic Candidate for Gout
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    Exploratory single-nucleus multiomics analysis of myeloid cell states associated with neoadjuvant chemotherapy response in pancreatic ductal adenocarcinoma
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    Use of the CRISPR-Cas9 system in Drosophila cultured cells to introduce fluorescent tags into endogenous genes
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    The phospholipid transporter PITPNC1 links KRAS to MYC to prevent autophagy in lung and pancreatic cancer
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    Isolating Ligand Steric Effects on Metal Ion Reduction and Gold Nanoparticle Formation Pathways Using Au(I)–Phosphine Complexes
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    Zonated cholesterol sensing by SIRT2 drives MASLD-HCC
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    طرز تهیه سالاد با پنیر موزارلا مدیترانه ای به سبک رستورانی
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    1. HabibehMajidi 19 Sep 2026
      طرز تهیه سالاد با پنیر موزارلا مدیترانه ای به سبک رستورانی

      اینجا گفتی مدیترانه ای بعد تو پاراگراف اول گفتی ایتالیایی! اینا خیلی مهمه بالاخره مال کجاست. منبع هم نداره این رسپی

    2. HabibehMajidi 19 Sep 2026
      ریحان تازه خیلی سریع تیره و پژمرده می‌شود، به همین دلیل بهتر است آن را با چاقوی تیز خرد نکنید و بیشتر با دست تکه‌تکه کنید. این کار باعث می‌شود عطر ریحان بهتر حفظ شده و ظاهر آن هم تازه‌تر باقی بماند.

      با چیزی که تو مراحل گفتی همخونی نداره این جاش همون بالاست به عنوان یک نکته در همون مرحله

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  22. www.youtube.com www.youtube.com
    Des policiers à la fac | Documentaire | ARTE
    1
    1. tanemika 19 Sep 2026

      Analyse Sociologique de l'Institution Policière : Regards de Praticiens

      Ce document de synthèse analyse les thématiques centrales issues des témoignages et des travaux de recherche menés par des fonctionnaires de police (commissaires, officiers, gardiens de la paix et CRS) engagés dans un cursus universitaire en sociologie.

      Il explore la tension entre l'identité institutionnelle, la réalité du terrain et la déconstruction analytique des pratiques professionnelles.

      Résumé Exécutif

      L'immersion de fonctionnaires de police dans la discipline sociologique révèle une fracture profonde entre l'image institutionnelle et la réalité vécue.

      Les principaux enseignements mettent en lumière :

      • Une rupture nécessaire avec le "sens commun" : L'apprentissage du "pas de côté" sociologique oblige les agents à transformer leurs expériences vécues en objets de recherche objectifs, délaissant le "nous" institutionnel pour une analyse critique.

      • Un décalage entre marketing et réalité : L'institution privilégie une image de prestige (unités d'élite) pour le recrutement, au détriment de la valorisation des missions quotidiennes de sécurité publique, souvent plus complexes et éprouvantes.

      • Une souffrance invisible : Derrière l'armure professionnelle et le déni hiérarchique (notamment sur la question du suicide), s'exprime un épuisement professionnel ("ras-le-bol") lié à une perte de sens et à une pression politique axée sur le chiffre.

      • Des enjeux de diversité occultés : Les questions de genre (« femmes patriarchées ») et d'origine sociale (transfuges de classe) créent des tensions internes et des sentiments d'illégitimité au sein même du corps policier.

      I. La Déconstruction du Raisonnement Policier par la Sociologie

      Le passage de l'action policière à l'analyse sociologique impose une transformation radicale de la vision du monde des agents.

      Du Problème Social au Problème Sociologique

      La sociologie ne cherche pas à résoudre les problèmes tels qu'ils sont définis par l'espace politico-médiatique.

      Elle définit ses propres objets de manière autonome.

      • L'autonomie de pensée : Le travail sociologique consiste à déplacer le regard pour sortir des schémas de pensée intégrés ("chevillés au corps").

      • La sociologie comme émancipation : Citant Pierre Bourdieu, les intervenants rappellent que la sociologie est un "sport de combat" utilisé pour se défendre et une voie vers l'émancipation intellectuelle.

      L'Objectivation de l'Expérience Personnelle

      Les policiers sont formés à parler au nom de l'institution ("le nous").

      La sociologie les contraint à utiliser le "je" pour ensuite l'objectiver.

      • La trajectoire individuelle : Une expérience personnelle (ex: être une femme lesbienne ou issue d'un milieu rural dans la police) rencontre des trajectoires collectives.

      • Le pas de côté : Il s'agit de chercher des explications à des sentiments (comme celui d'avoir "mauvaise presse") non pas chez les autres (médias, citoyens), mais au sein même de l'organisation policière.

      II. Identité, Genre et Rapports de Classe

      Le contexte source souligne des tensions internes liées aux origines sociales et au genre des fonctionnaires.

      Le Concept de "Femme Patriarchée"

      Une réflexion est menée sur la place des femmes dans une institution perçue comme masculine, voire masculiniste.

      • Assimilation des codes : Les femmes policières absorberaient les codes et usages de l'institution pour s'y intégrer et se faire accepter.

      • Tensions militantes : Des partenariats avec des associations féministes révèlent la méfiance initiale envers ces "femmes patriarchées" travaillant pour la police.

      Le Transfuge de Classe

      Certains hauts gradés expriment un sentiment d'illégitimité dû à leur origine sociale.

      • Décalage CSP : Un commissaire issu d'un milieu rural évoque la violence des remarques de ses pairs ("Tu n'es qu'une paysanne").

      • Absence de codes : Le sentiment d'être "nulle part chez soi", entre un milieu d'origine modeste et un corps d'encadrement supérieur aux codes très fermés.

      III. Réalités Opérationnelles et Pressions Politiques

      L'analyse met en évidence une distorsion entre les priorités politiques et l'efficacité réelle du travail de terrain.

      La Rationalité du Chiffre vs Enquêtes de Fond

      Les services d'investigation (notamment les stupéfiants) sont soumis à des impératifs de visibilité.

      • Priorisation des réseaux visibles : La hiérarchie impose de cibler les points de deal où les résultats sont "chiffrables" et "vendables" politiquement, au risque de parasiter des enquêtes de longue haleine plus ambitieuses.

      • Écarts de revenus illicites : Une comparaison est établie entre les marchés illégaux : | Type de fraude/trafic | Estimation du chiffre d'affaires annuel | | :--- | :--- | | Fraude et évasion fiscale | 60 à 80 milliards d'euros | | Trafic de drogue | 2 à 4 milliards d'euros |

      Le Marketing d'État

      L'institution est critiquée pour son usage de la communication, transformant parfois les unités (comme la CRS 82) en "outils marketing".

      • Recrutement "rêvé" : On montre des unités d'élite au lieu de la réalité de la "police secours" (gestion de l'ivresse publique, conflits de voisinage).

      • Déni de la réalité : L'incapacité de l'institution à assumer la réalité du métier rend le quotidien des agents difficile à concilier avec leurs motivations initiales de service public.

      IV. L'Usage de la Force et la Relation Police-Population

      La sociologie permet d'interroger la légitimité de la violence et l'évolution des tensions sociales.

      La Violence Légitime et l'Autocontrainte

      • Confusion des rôles : Certains agents considèrent à tort que la violence légitime est à leur "bon vouloir", alors qu'elle appartient à l'institution.

      • Baisse de la tolérance à la violence : On observe une augmentation de l'intolérance à la violence chez les jeunes recrues (qui ne supportent plus d'être visées comme symboles politiques) et chez les manifestants (qui documentent les usages non réglementaires des armes comme le LBD).

      • Vision unilatérale : Dans le maintien de l'ordre, une vision s'impose souvent : le manifestant est perçu comme illégitime, effaçant les opinions personnelles du fonctionnaire au profit de la vision institutionnelle.

      Contrôle Social et Inégalités

      L'analyse des données de condamnation pour usage de stupéfiants révèle des biais systémiques :

      • Les classes moyennes et supérieures consomment davantage, mais les classes populaires sont plus souvent condamnées.

      • Cela s'explique par l'organisation du quadrillage policier et la fréquence des contrôles d'identité dans l'espace public (jusqu'à 20 fois plus de chances d'être contrôlé selon le profil).

      V. Souffrance Institutionnelle et Vulnérabilité

      Un thème récurrent est celui de la "fissure" de l'armure policière face au traumatisme et à l'indifférence hiérarchique.

      La Gestion des Émotions

      • Le masque professionnel : Les policiers doivent contenir leurs émotions sur le terrain pour rester "professionnels".

      • Le besoin de parole : Le chercheur (sociologue) devient parfois un confident inattendu, car il offre une écoute que les collègues ou l'institution ne permettent pas.

      Le Drame du Suicide

      Le suicide est traité de manière incisive comme le symptôme d'une "désespérance" profonde.

      • Le "parapluie de l'irresponsabilité" : La hiérarchie tend à qualifier systématiquement les suicides de "problèmes personnels" pour dégager la responsabilité de l'administration.

      • Abandon institutionnel : Des témoignages font état d'un sentiment d'abandon après des accidents de carrière ou des problèmes de santé, menant à une rupture de confiance envers l'institution.

      Conclusion : La Sociologie comme Outil de Réflexion Professionnelle

      Le document conclut que la démarche sociologique, bien que déstabilisante, est capitale pour l'autonomie des fonctionnaires.

      Elle permet de passer d'un "métier passion" à une compréhension structurelle des dysfonctionnements, offrant ainsi une perspective de changement ou, à défaut, une meilleure connaissance de soi au sein d'un système contraignant.

      La sociologie n'est pas là pour réformer de l'extérieur, mais pour offrir les armes intellectuelles nécessaires à la compréhension de l'humain et de la complexité sociale.

      arte documentaire sociologie forces de l'ordre police 2026 vidéo violence
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  23. www.info.gov.hk www.info.gov.hk
    《香港第一個五年規劃》和二○二六年《施政報告》記者會答問內容（附圖／短片）
    1
    1. AnitaLi 19 Sep 2026
      「十五五」規劃

      「十五五」即係第十五個五年規劃，主要講國家喺2026年至2030年呢五年，經濟、科技、民生等方面嘅發展方向同目標。

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  24. www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov
    PERIPAPILLARY ATROPHY IN STARGARDT DISEASE
    1
    1. Vibhor 19 Sep 2026
      Case 4A 52-year-old male was examined for declining vision OS over the past few months. He was previously clinically diagnosed with STGD 7 years before presentation. Family history was not significant for ocular disease. Best-corrected visual acuity measured 20/100 OD and 20/70 OS. Spherical refractive error measured −3.00 OD and −3.25 OS. Anterior segment examination was unremarkable and applanation tonometry measured 17 mmHg OD and 14 mmHg OS. Posterior segment examination was significant for central atrophy and classic peripheral pisciform flecks sparing the peripapillary regions OU (Figure 4, A and B). Autofluorescence imaging demonstrated inner atrophic flecks and outer hyperautofluorescent flecks. Moderate peripapillary hypoautofluorescence, but not atrophy, was present, likely secondary to the patient’s myopia (Figure 4, C and D). Genotyping revealed two heterozygous ABCA4 mutations, P1380L and S1696N.Open in a separate windowFig. 4Case 4. STGD mutation IVS40 + 5G>A. A, Color Photo OU. B, Red-Free Photo OU reveal central atrophy and classic peripheral pisciform flecks sparing the peripapillary regions OU. C, Autofluorescence OD. D, Autofluorescence OS show that the innermost flecks are hypoautofluorescent, consistent with atrophy, whereas the outermost flecks are hyperautofluorescent, demonstrating excess lipofuscin. There is moderate peripapillary hypoautofluorescence that is not as dark as this patient’s central atrophy or the peripapillary atrophy of Case 1. This finding may thus be due to the patient’s myopia.

      Case#: Hwang Case 4, male, 52yo at report, 45yo at onset

      DiseaseAssertion: Stargardt

      FamilyInfo: Family history was not significant for ocular disease.

      CasePresentingHPOs: HP:0000545

      CaseHPOFreeText: declining vision OS, BCVA was 20/100 OD and 20/70 OS. Spherical refractive error measured −3.00 OD and −3.25 OS. Posterior segment examination was significant for central atrophy and classic peripheral pisciform flecks sparing the peripapillary regions OU (Figure 4, A and B). Autofluorescence imaging demonstrated inner atrophic flecks and outer hyperautofluorescent flecks. Moderate peripapillary hypoautofluorescence, but not atrophy, was present (Figure 4, C and D).

      CaseNotHPOs: HP:0500087

      CaseNotHPOFreeText:

      GenotypingMethod: Genotyping was performed by the ABCR400 microarray followed by direct sequencing to confirm identified variants.

      PreviouslyPublished: n/a

      Variant: P1380L and S1696N

      ClinVar: 7904

      CAID: CA129033

      SupplementalData: n/a

      ClinVarID: 7904 CA129033 CaseInfo Individual inferred_gene_hgnc:34 inferred_gene_source:CAID ClinGen ABCA4 Annotations
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    ncbi.nlm.nih.gov/pmc/articles/PMC2743754/
  25. pmc.ncbi.nlm.nih.gov pmc.ncbi.nlm.nih.gov
    Mutations of the retinal specific ATP binding transporter gene (ABCR) in a single family segregating both autosomal recessive retinitis pigmentosa RP19 and Stargardt disease: evidence of clinical heterogeneity at this locus
    1
    1. Vibhor 19 Sep 2026
      Mutations of the retinal specific ATP binding transporter gene (ABCR) in a single family segregating both autosomal recessive retinitis pigmentosa RP19 and Stargardt disease: evidence of clinical heterogeneity at this locus

      PMID: 10874631

      Gene: ABCA4

      HGNC ID: 34

      Case#: patient 34, female

      DiseaseAssertion: STGD

      FamilyInfo: paternal first cousin with RP19, healthy father heterozygous for 1938-1 G>A splice mutation

      CasePresentingHPOs: HP:0007663, HP:0000608, HP:0000603,

      CaseHPOFreeText: yellowish flecks

      Genotyping Method: PRISMTM Ready Reaction Sequencing Kit on an automatic fluorometric DNA sequencer

      PreviouslyPublished: N/A

      Variant: NM_000350.3(ABCA4):c.1938-1G>A

      ClinVar: 99106 https://www.ncbi.nlm.nih.gov/clinvar/variation/99106/?term=%22ABCA4%22%5BGENE%5D+AND+%22(c.1938-1G%3EA)%22%5BVARNAME%5D

      gnomAD: 0.000002488 https://gnomad.broadinstitute.org/variant/1-94060760-C-T?dataset=gnomad_r4

      General ABCA4 HGNC:34 PMID:10874631 inferred_gene_hgnc:34 inferred_gene_source:hgnc_tag ClinGen ABCA4 Annotations
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    pmc.ncbi.nlm.nih.gov/articles/PMC1734380/
  26. www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov
    Detailed genetic characteristics of an international large cohort of patients with Stargardt disease: ProgStar study report 8
    1
    1. Vibhor 19 Sep 2026
      Supplementary data. bjophthalmol-2018-312064supp004.pdf

      This variant is found on pg 11 in proband 18034. Compound heterozygous for c.2588G>C p.Gly863Ala. Said to have Stargardt based on the following criteria: "(1) patients (at least 6 years old) with at least two ABCA4 variants or one ABCA4 variant associated with a typical STGD1 phenotype and (2) presence of a well-defined atrophic lesion with/without flecks at the most recent visit of at least 300 µm in diameter (the total area of all lesions <12 mm2)." No additional details provided

      CaseInfo Individual ClinVarID: 99455 CA227399 inferred_gene_hgnc:34 inferred_gene_source:CAID ClinGen ABCA4 Annotations
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    ncbi.nlm.nih.gov/pmc/articles/PMC6579578/
  27. onlinelibrary.wiley.com onlinelibrary.wiley.com
    Longitudinal follow-up of siblings with a discordant Stargardt disease phenotype
    1
    1. Vibhor 19 Sep 2026
      Patient 1 is 44 years old and presented in 1991 aged 23 with deteriorating central vision and visual acuity (VA) of 6/36 in the right eye and 6/60 in the left. Fundus photography in 1994 identified bilateral numerous yellowish-white flecks at the posterior pole (Fig. 1). In 2003, her VA was 6/60 in each eye, with bilateral macular atrophy surrounded by flecks (Fig. 1). Autofluorescence (AF) imaging in 2005 detected a localized low signal at the macula with numerous foci of abnormal signal (Fig. 1). By 2008, the macular atrophy had enlarged and flecks were less apparent.

      Case#: Female, age 44 years old

      DiseaseAssertion: Discordant STGD phenotype

      FamilyInfo: Information revolving the sister of this patient is given as well as they both have a discordant STGD phenotype. Additionally, it mentions that the parents each harboured a mutation but were asymptomatic/had normal examination results.

      CasePresentingHPOs: HP:0001141, HP:0007401, HP:0030602

      CaseHPOFreeText: At 23 central vision was deteriorating and patient had a VA of 6/36 in the right eye and 6/60 in the left. Through fundus photography, bilateral yellow/white flecks were found at the posterior pole. 12 years later, her VA was retested and it was 6/60 in both eyes. After autofluorescnece (AF) imaging was done, there was localized low signal at the macula found with abnromal foci. In 2008 her macular atrophy had enlarged and the flecks were less apparent.

      CaseNotHPOs: N/a

      CaseNotHPOFreeText: In this article there was not a phenotype presented that was normal.

      CasePreviousTesting: It mentioned that there were two previously reported variants on the same allele detected in the siblings and one unique novel variant on the second allele for this patient. However, the testing they used was not listed, it just stated that the variants were found through sequencing. For this patient the variants were p.L541P/p.A1038V and p.R881C.

      GenotypingMethod: Just mentioned sequencing and ABCA4 screening to look for two variants p.L541V and p.A1038V and a third novel variant p.R881C.

      PreviouslyPublished: N/a

      Variant: 1) NM_000350.3(ABCA4):c.1622T>C (p.Leu541Pro) 2) NM_000350.3(ABCA4):c.3113C>T (p.Ala1038Val) 3) N/a

      ClinVar ID: 1) 99067 2) 7894 3) N/a

      **CAID: ** 3) Because there was not a reference or alternate allele provided in this article I was unable to find a CAID for p.R881C.

      gnomAD: 1) Highest minor allele frequency was 0.00017 (https://www.ncbi.nlm.nih.gov/clinvar/variation/99067/) 2) Highest minor allele frequency was 0.00188 (https://www.ncbi.nlm.nih.gov/clinvar/variation/7894/) 3) N/a

      SupplementalData: Figure 1 had information regarding imaging and other testing done on the patient that is vital for phenotypic characterization. Also, it mentions a variant known as p.R881C, but was unable to find anything on ClinVar or gnomAD.

      Gene:ABCA4 HGNC:34 InheritancePattern:AutosomalRecessive (6)DiseaseEntity:STGD1 AlleleOrigin:Somatic Zygosity:CompoundHeterozygous (17)DecreasedCentralVA (1)MacularFlecks (2)FundusAutofluorescence (13) MacularAtrophy FamilyInfo inferred_gene_hgnc:34 inferred_gene_source:hgnc_tag ClinGen ABCA4 Annotations
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    onlinelibrary.wiley.com/doi/10.1111/aos.12280
  28. www.ajo.com www.ajo.com
    mmc1.pdf
    1
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    ajo.com/cms/10.1016/j.ajo.2020.06.027/attachment/2c3c8baa-ae3a-4cb6-a3ad-ae429569a986/mmc1.pdf
  29. journals.sagepub.com journals.sagepub.com
    Novel ABCA4 mutation leads to loss of a conserved C-terminal motif: implications for predicting pathogenicity based on genetic testing - Nutsuchar Wangtiraumnuay, Jenina Capasso, Mai Tsukikawa, Alex Levin, Esther Biswas-Fiss, 2018
    1
    1. Vibhor 19 Sep 2026
      We report an 11-year-old girl

      Case#: 11 year old female

      DiseaseAssertion: Stargardt’s Disease

      ParentalTesting: She was the product of an uncomplicated pregnancy born to a healthy Filipino mother and Italian/Irish father with no known family history of ocular disease. The mother and father were asymptomatic but not examined. Segregation analyses showed that both parents are asymptomatic carriers.

      CasePresentingHPOs: HP:0007754, HP:0011462, HP:0008035

      CasePhenotypeFreeText: The ABCA4 gene, when mutated, results in a spectrum of retinal degeneration, including Stargardt macular dystrophy, fundus flavimaculatus, autosomal recessive retinitis pigmentosa, and cone-rod dystrophy (1). Over 800 disease-associated ABCA4 gene mutations have been reported.

      CaseNotHPOs: N/A

      CaseNotPhenotypeFreeText: N/A

      CasePreviousTesting: The proband underwent a full consultative ophthalmic examination at the Ocular Genetics Clinic at Wills Eye Hospital, including visual acuity, slit-lamp, and dilated fundus examination. Fundus autofluorescence and spectral-domain optical coherence tomography (Spectralis; Heidelberg Engineering), Goldmann visual field (Octopus 900 perimeter; Haag-Streit International), and intravenous fluorescein angiography were obtained. Full-field electroretinogram (Espion; Diagnosys LLC) and multifocal electroretinogram (Veris V.6.4.3; EDI Inc.) were performed in accordance with the International Society of Clinical Electrophysiology and Vision standards. Best-corrected visual acuity was 20/125 in the right eye and 20/200 in the left eye. The patient demonstrated eccentric fixation. Pupillary responses were normal. Slit-lamp examination was normal. Fundus examination revealed healthy optic nerves and retinal blood vessels, bilateral macular geographic pigmentary stippling with subretinal flecks in and around this area, and a blunted internal limiting membrane reflex (Fig. 1). Peripheral retina was normal.

      GenotypingMethod: Genotyping microarray chips for ABCA4 can identify >98% of the most common mutations. In this report, we describe 2 novel ABCA4 variants in a patient with Stargardt disease. Bioinformatic and in silico analysis of the functional consequences of these variants provided compelling evidence for pathogenicity.

      Variant: c.850_857delATTCAAGA and c.6184_6187delGTCT

      CAID: CA10604079 and CA10604078

      MultipleGeneVariants: N/A

      PreviouslyPublished: N/A

      AdditionalInfo: Bioinformatic assessment of the c.850_857delATTCAAGA mutation showed that it resulted in a truncated 317 amino acid polypeptide, devoid of several essential domains of the ABCA4 transporter. The c.6184_6187delGTCT mutation led to a premature stop codon at the C-terminal end of the protein, resulting in a loss of a total of 161 amino acid residues. Although less than 7% of the protein was absent, the important VFVNFA motif, present within the last 30 amino acids of the NBD2 domain, was deleted (Fig. 2). This motif is known to be critical to ABCA4 protein function, is highly conserved among members of the ABCA transporter subfamily, and has also been linked to Tangier disease in the ABCA1 protein (9). Removal of this motif in ABCA4 leads to a loss of retinal stimulated ATPase in vitro and energy transduction of the transporter (9, 10). Protein modeling predicted a loss of an essential β-sheet, which significantly altered its structure. The NBD domains are sites of ATP hydrolysis that provide energy for transport of R-PE through rod outer segment membranes. Enzymatic studies suggest that the NBD2 domain in particular provides energy necessary for translocation of retinal derivatives generated in the visual cycle. The structural changes in NBD2 would affect ABCA4 transporter’s ability to transport retinoids, leading to accumulation of cytotoxic lipofuscin in RPE cells and ultimately photoreceptor cell death.

      Gene:ABCA4 DiseaseAssertion:Starghardt'sDisease FundusFlavimaculatus ConeRodDystrophy Zygosity:CompoundHeterozygous HGNC:34 AdditionalInfo CAID:CA10604078 CAID:CA10604079 inferred_gene_hgnc:34 inferred_gene_source:hgnc_tag ClinGen ABCA4 Annotations
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    journals.sagepub.com/doi/10.5301/ejo.5001019
  30. pubmed.ncbi.nlm.nih.gov pubmed.ncbi.nlm.nih.gov
    Application of targeted exome and whole-exome sequencing for Chinese families with Stargardt disease
    1
    1. Vibhor 19 Sep 2026
      A cohort of 12 unrelated STGD families diagnosed on the basis of clinical manifestations underwent analysis by targeted exome or whole-exome sequencing. Bioinformatics analysis, Sanger sequencing, and cosegregation analysis of available family members were used to validate sequencing data and confirm the presence of disease-causing genes. Results: Using targeted exome and whole-exome sequencing, we found that eight families had disease-causing variants in the ABCA4 gene, one family had only one heterozygous variant in the ABCA4 gene, and the remaining three families have not been identified with any disease-causing variants for STGD. We identified 15 variants in the ABCA4 gene; of these, five variants have not been previously described for STGD.

      Unable to annotate on PDF, so annotating here.

      Case#: Proband #4, male, Chinese, onset at 12yo

      DiseaseAssertion: stargardt

      FamilyInfo: parents are deceased, so phase is unknown. daughter is an unaffected carrier of this variant

      CasePresentingHPOs: HP:0025147, HP:0011507, HP:0000608

      CaseHPOFreeText: BCVA=0.3/CF, mean retinal nerve fiber layer(µm)=167/154, Visual field(mean deviation)= 7.52/NA, fundus fluorescein angiography=type C (a pattern of speckled hypofluorescence and hyperfluorescence without central hypofluorescence)

      CaseNotHPOs:

      CaseNotHPOFreeText:

      PreviouslyPublished: n/a

      Variant: c.6289C > T p.(Pro2097Ser); c.4720G > T p.(Glu1574*) on targeted exome sequencing or WES

      ClinVar: 2202780; 1460063

      CAID: CA341277622; CA341283936

      SupplementalData: n/a

      CaseInfo Individual ClinVarID: 2202780 CA341277622 ClinVarID: 1460063 CA341283936 inferred_gene_hgnc:34 inferred_gene_source:CAID ClinGen ABCA4 Annotations
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    pubmed.ncbi.nlm.nih.gov/31674661/
  31. www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov
    Personalized genetic counseling for Stargardt disease: Offspring risk estimates based on variant severity
    1
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    ncbi.nlm.nih.gov/pmc/articles/PMC8948157/
  32. www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov
    From the Cover: Worldwide carrier frequency and genetic prevalence of autosomal recessive inherited retinal diseases
    2
    1. Vibhor 19 Sep 2026
      To determine the overall CF for all AR-IRD–causing mutations in different subpopulations, we initially calculated CF for each of the 10,044 likely pathogenic variants in each subpopulation (SI Appendix, Tables S2 and S3).

      This variant is found in Supplemental Table S3, but this table lists frequencies and does not give case information

      NoEvidence SupplementalTable CA341283936 ClinVarID: 1460063 inferred_gene_hgnc:34 inferred_gene_source:CAID ClinGen ABCA4 Annotations
    2. Vibhor 19 Sep 2026
      To determine the overall CF for all AR-IRD–causing mutations in different subpopulations, we initially calculated CF for each of the 10,044 likely pathogenic variants in each subpopulation (SI Appendix, Tables S2 and S3).

      This variant is found in Supplemental Table S3, but this table lists frequencies and does not give case information

      SupplementalTable NoEvidence CA227399 ClinVarID: 99455 inferred_gene_hgnc:34 inferred_gene_source:CAID ClinGen ABCA4 Annotations
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    ncbi.nlm.nih.gov/pmc/articles/PMC7007541/
  33. pmc.ncbi.nlm.nih.gov pmc.ncbi.nlm.nih.gov
    Novel ABCA4 compound heterozygous mutations cause severe progressive autosomal recessive cone-rod dystrophy presenting as Stargardt disease
    1
    1. Vibhor 19 Sep 2026
      The proband

      Case#: two affected sisters

      DiseaseAssertion: Stargardt Disease

      FamilyInfo: compound heterozygotes for the mutations. Unaffected family members did not carry either or had one of the two mutations.

      CasePresentingHPOs: NR

      CaseHPOFreeText: NR

      CaseNotHPOs: NR

      CaseNotHPOFreeText: NR

      Genotyping Method: ABCA4 408 microsatellite

      PreviouslyPublished: NR

      Variant: NM_000350.3(ABCA4):c.5018+2T>C , NM_000350.3(ABCA4):c.655A>T

      ClinVar: 265008, 632118

      CAID: CA10588304, CA645372240

      SupplementalData: NR

      ClinVar: 265008 Variant: c.655A>T, c.5312+3A>T inferred_gene_hgnc:34 inferred_gene_source:CAID ClinGen ABCA4 Annotations
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    pmc.ncbi.nlm.nih.gov/articles/PMC2665199/
  34. www-sciencedirect-com.libproxy.lib.unc.edu www-sciencedirect-com.libproxy.lib.unc.edu
    Comprehensive genetic analysis reveals the mutational landscape of ABCA4-associated retinal dystrophy in a Chinese cohort
    1
    1. Vibhor 19 Sep 2026
      We identified 255 patients (87.9 %) harboring biallelic ABCA4 variants, 27 probands (9.3 %) with two or three variants but lacking familial segregation analysis, and eight patients (2.8 %) with monoallelic ABCA4 variants (Supplemental Table S4). We detected 268 distinct ABCA4 variants, consisting of 114 missense, 35 nonsense, 34 frameshift deletion or insertion, 31 canonical splice variants, 13 noncanonical splice site variants, 9 in-frame deletion or insertion, 9 DIVs, 4 structural variations, and 19 complex variants (Fig. 2).

      Case#: Patient#010455, Chinese, male, 18yo at onset

      DiseaseAssertion: stargardt

      FamilyInfo: n/a

      CasePresentingHPOs: STGD1 diagnosis based on the following criteria: "a bilateral central vision defect; fundus displaying a beaten-bronze appearance and/or orange-yellow flecks in the retina from the macula to the midperiphery; fluorescein angiography presenting with a typical dark choroid; and normal to subnormal ERG results." BCVA=0.01/ 0.01

      CaseHPOFreeText:

      CaseNotHPOs:

      CaseNotHPOFreeText:

      PreviouslyPublished: n/a

      Variant: p.P2097S; c.4906_4908del p.(Asn1636del) phase unknown

      ClinVar: 2202780;

      CAID: CA341277622;

      SupplementalData: supplementary table S4 has phenotype information

      CaseInfo Individual CA341277622 ClinVarID: 2202780 SupplementalTable inferred_gene_hgnc:34 inferred_gene_source:CAID ClinGen ABCA4 Annotations
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    www-sciencedirect-com.libproxy.lib.unc.edu/science/article/pii/S037811192300673X
  35. onlinelibrary.wiley.com onlinelibrary.wiley.com
    Fine central macular dots associated with childhood-onset Stargardt Disease
    1
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    onlinelibrary.wiley.com/doi/10.1111/aos.12259
  36. pmc.ncbi.nlm.nih.gov pmc.ncbi.nlm.nih.gov
    Novel mutations in c2orf71 causing an early onset form of cone-rod dystrophy: A molecular diagnosis after 20 years of clinical follow-up
    1
    1. Vibhor 19 Sep 2026
      a 45-year-old man

      Case#: a 45-year-old man from Sardinia, Italy

      DiseaseAssertion: Cone rod dystrophy

      FamilyInfo: Five members, this patient is the only one affected by CRD

      CasePresentingHPOs: HP:0000505, HP:0007663, HP:0000603, HP:0001123, HP:0000608, HP:0007401, HP:0011504, HP:0000548, HP:0030329, HP:0000543

      CaseHPOFreeText: 1998: Subacute central vision loss in both eyes, choroidal and RPE atrophy surrounding left fovea and small white patches of atrophy around right fovea. Pale appearance of optic disc in both eyes. Punctate retinal pigment epitheliopathy observed bilaterally in midperipheral retina, hyperfluorescent macular regions suggesting bull's eye maculopathy. Paracentral ring scotoma, surrounded by a relative annular scotoma, early and predominant involvement of photopic over scotopic responses; 2018: BCVA was bilateral light perception with visual field extinction. FAF showed a central round area of decreased autofluorescence corresponding to area of macular atrophy, surrounded by an area of relatively increased autofluorescence. Several roundish areas of reduced autofluorescence in midperipheral retina. Severe macular atrophy surrounded by a ring of preserved RPE in both eyes. Sparse pigmentary deposits in midperipheral retina of both eyes. Severe bilateral retinal thinning with disappearance of external retinal layers. Outer retina tubulations

      CaseNotHPOs: HP:0025148

      CaseNotHPOFreeText: No pigment deposits on optic disc, no dark choroid

      Genotyping Method: Candidate gene approach on ABCA4 followed by whole exome sequencing

      PreviouslyPublished: NR

      Variant: NM_000350, c.4535C>G, p.P1512R

      ClinVar: 99291

      CAID: CA227203

      SupplementalData: Patient's healthy brother showed the same molecular condition for ABCA4. Patient also has 2 novel frameshift mutations in C2orf71.

      InheritancePattern:AutosomalRecessive Zygosity:Heterozygous DiseaseEntity:Cone-rod-dystrophy Mutation:Missense CAID:CA227203 inferred_gene_hgnc:34 inferred_gene_source:CAID ClinGen ABCA4 Annotations
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    pmc.ncbi.nlm.nih.gov/articles/PMC6887784/
  37. pubmed.ncbi.nlm.nih.gov pubmed.ncbi.nlm.nih.gov
    Whole exome sequencing detects homozygosity for ABCA4 p.Arg602Trp missense mutation in a pediatric patient with rapidly progressive retinal dystrophy
    1
    1. Vibhor 19 Sep 2026
      An eight year-old Hispanic female

      Case#: An 8-year old Hispanic female

      DiseaseAssertion: Whole exome sequencing identified a homozygous ABCA4 missense variant (p.Arg602Trp) that has been identified as a Stargardt Disease mutation

      FamilyInfo: consanguinity, her parents being first cousins, no family history of blindness. Familial cosegregation analysis was used, with both parents being heterozygous carriers.

      CasePresentingHPOs: HP:0000529, HP:0000662, HP:0000556, HP:0002017,HP:0008046, HP:0031528, HP:0003678

      CaseHPOFreeText: rapidly progressive vision loss, nyctalopia and retinal dystrophy, bilateral decreased vision following a febrile gastrointestinal illness with nausea and vomiting, Initial visual acuity was 20/60 at distance and 20/30 at near in both eyes, after 2 years visual acuities of 20/200 at distance in both eyes, attenuated vessels and multiple subretinal blister-like elevations, Cycloplegic retinoscopy detected very mild hyperopia and astigmatism in both eyes (OD: + 1.00 sphere + 1.00 cylinder axis 110 degrees; OS: + 0.75 sphere + 0.50 cylinder axis 60 degrees)

      CaseNotHPOs: NR

      CaseNotHPOFreeText: no evidence of a diffuse post-infectious/inflammatory process

      Genotyping Method: DNA analysis by whole exomic sequencing

      PreviouslyPublished: No

      Variant: NM_000350.3:c.1804C>T

      ClinVar:99084

      CAID:CA226932

      SupplementalData:

      DiseaseEntity:IRD Zygosity:Homozygous FamilyInfo ClinVarID:99084 CAID:CA226932 inferred_gene_hgnc:34 inferred_gene_source:CAID ClinGen ABCA4 Annotations
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    pubmed.ncbi.nlm.nih.gov/24444108/
  38. www.gimjournal.org www.gimjournal.org
    Resolving the dark matter of ABCA4 for 1054 Stargardt disease probands through integrated genomics and transcriptomics
    1
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    gimjournal.org/article/S1098-3600(21)01183-7/fulltext
  39. pmc.ncbi.nlm.nih.gov pmc.ncbi.nlm.nih.gov
    CLINICAL CHARACTERIZATION OF STARGARDT DISEASE PATIENTS WITH THE p.N1868I ABCA4 MUTATION
    1
    1. Vibhor 19 Sep 2026
      son (the proband of Family #3, pedigree in Figure 1C)

      Case#: Male, Family#3, Proband M1, M2: II,1 on pedigree

      DiseaseAssertion: STGD

      FamilyInfo: mother of proband has p.N18681 and p.P1380L mutations and is asymptomatic with no changes to NIR-AF and SD-OCT. Treated with 400mg of hydroxychloroquine for lupus prior to imaging. Non-affected father.

      CasePresentingHPOs:HP:0007663, HP:0000493

      CaseHPOFreeText: Proband has reduced visual acuity and issues reading with BCVA 20/200 in R.E and 20/50-2 in L.E. Oval foveal lesions with stage 2 flecks. Visual acuity reducing starting at age 10.

      CaseNotHPOs: n/a

      CaseNotHPOFreeText: n/a

      Genotyping Method: Genotyping performed at Columbia University, sequencing technology used is not disclosed.

      PreviouslyPublished: n/a

      Variant: M1:p.P1380L, complex allele: M2: p.N18681 and IVS38:c.5461-10T>C. M3: c.4139C>T(p.P1380L)

      ClinVar: M1) 99390 M2) 99067 M3) Variation ID: 7904

      CAID: n/a

      SupplementalData: Fig 1: Pedigree illustrating ABCA4 variants and the associated Stargardt phenotype for 5 families. Proband Labeled w/ white arrow for each family. Fig 2: retinal scan measuring melanin in 4 patients of family 2. Panel shows bull's-eye ring of RPE atropy. Fig 3: Macular SD-OCT line profile from b-scans. Reflectivity plotted against function of retinal depth. Table 1: table shows patients with p.N18681 variant, type of mutation, and pathogenicity class. Table 2: Patients, age on-set and first symptom

      Gene: ABCA4 HGNC: 34 InheritancePattern: autosomal recessive AllelicOrigin: Somatic Zygosity: CompoundHeterozygous FamilyInfo inferred_gene_hgnc:34 inferred_gene_source:Gene_Name ClinGen ABCA4 Annotations
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    pmc.ncbi.nlm.nih.gov/articles/PMC6548695/pdf/nihms-1032320.pdf
  40. pmc.ncbi.nlm.nih.gov pmc.ncbi.nlm.nih.gov
    Subretinal Fibrosis in Stargardt's Disease with Fundus Flavimaculatus and ABCA4 Gene Mutation
    1
    1. Vibhor 19 Sep 2026
      Case 1

      Case#: Case1, Sex:Female, Age:35

      DiseaseAssertion: STGD

      FamilyInfo: n/a

      CasePresentingHPOs: n/a

      CaseHPOFreeText: Clinical Notes: the patient reported an ocular trauma in the right eye, which required hospitalization and caused sudden loss of vision at the age of 9 years. In 1998, at our first observation, visual acuity was 20/1,000 in the right eye and 20/600 in the left eye.

      CaseNotHPOs:n/a

      CaseNotHPOFreeText: n/a

      Genotyping Method: genetic analysis

      PreviouslyPublished: n/a

      Variant: Variant is a heterozygous mutation given as (N965S/G1961E); NM_000350.3(ABCA4):c.2894A>G (p.Asn965Ser) /NM_000350.3(ABCA4):c.5882G>A (p.Gly1961Glu)

      ClinVar: Variation ID: 236096 / Variation ID: 7888

      SupplementalData: n/a

      Gene:ABCA4 HGNC:34 PMID:3341817 ClinVarID:236096 UnregisteredVariant DiseaseEntity:STGD1 Zygosity:Heterozygous inferred_gene_hgnc:34 inferred_gene_source:hgnc_tag ClinGen ABCA4 Annotations
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    pmc.ncbi.nlm.nih.gov/articles/PMC3551412/
  41. pmc.ncbi.nlm.nih.gov pmc.ncbi.nlm.nih.gov
    Novel compound heterozygous mutations in ABCA4 in a Chinese pedigree with Stargardt disease
    1
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    pmc.ncbi.nlm.nih.gov/articles/PMC5204459/
  42. www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov
    Predicting Progression of ABCA4-Associated Retinal Degenerations Based on Longitudinal Measurements of the Leading Disease Front
    1
    1. Vibhor 19 Sep 2026
      the model would predict foveal disease in the first decade of life for three alleles (P68L;G1961E, L541P;A1038V, and T1019M)

      Case#: Cideciyan Case #86, male, 20.5yo at report

      DiseaseAssertion: "clinical diagnosis within the spectrum of Stargardt disease or cone–rod dystrophy caused by ABCA4 mutations."

      FamilyInfo: Parental segregation of the reported alleles confirmed. P87 is the proband's sibling, affected, same genotype

      CasePresentingHPOs:

      CaseHPOFreeText: LDF eccentricity along principal meridians [deg]: superior=16.9, inferior=11.7, temporal=18.9, inner nasal=9.6, outer nasal=18.9

      CaseNotHPOs:

      CaseNotHPOFreeText:

      GenotypingMethod: NGS

      PreviouslyPublished: PMID: 24550365

      Variant: c.203 C>T p.Pro68Leuc.5882 G>A p.(Gly1961Glu); c.5882 G>A p.(Gly1961Glu). Phase confirmed.

      ClinVar: 99113

      CAID: CA226972

      SupplementalData: table s1

      CaseInfo Individual SupplementalTable ClinVarID: 99113 CA226972 inferred_gene_hgnc:34 inferred_gene_source:CAID ClinGen ABCA4 Annotations
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    ncbi.nlm.nih.gov/pmc/articles/PMC4572941/
  43. search.brave.com search.brave.com
    Brave Search
    2
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    search.brave.com/search
  44. lawphil.net lawphil.net
    R.A. 386
    1
    1. romeopateno 19 Sep 2026
      An accepted unilateral promise to buy or to sell a determinate thing for a price certain is binding upon the promisor if the promise is supported by a consideration distinct from the price.

      Binding only when the consideration is distinct from the purchase price.

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    lawphil.net/statutes/repacts/ra1949/ra_386_1949.html
  45. human.libretexts.org human.libretexts.org
    2.2: Types of Claims to Look out for
    2
    1. nysalichau 19 Sep 2026
      Raising the minimum wage will force many small businesses to lay off workers.

      I don't really see this as a reason not to raise minimum wage. Wouldn't this be a small consequence compared to workers needing to work multiple jobs to make ends meet?

    2. nysalichau 19 Sep 2026
      _____________is mediocre/average/decent/acceptable.

      Claims of Value seems to be having an opinion, which makes sense why it is so easy to spot. An example would be: "Human rights are more important than border security."

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    human.libretexts.org/Bookshelves/Composition/Advanced_Composition/How_Arguments_Work_-_A_Guide_to_Writing_and_Analyzing_Texts_in_College_(Mills)/02:_Reading_to_Figure_out_the_Argument/2.02:_Types_of_Claims_to_Look_out_for
  46. spada.uns.ac.id spada.uns.ac.id
    9780321786555.pdf
    1
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    spada.uns.ac.id/pluginfile.php/221008/mod_resource/content/1/ProbabilityStatistics_for_EngineersScientists(9th_Edition)_Walpole.pdf
  47. hypothes.is hypothes.is
    Hypothesis
    1
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    hypothes.is/welcome/93a447e023bb2db5
  48. new.contest.yandex.ru new.contest.yandex.ru
    H. Strategy tetris — Тренировки 10.0 - 2.3. Реализация кучи
    1
    1. devilboi 19 Sep 2026

      Как будто не важен порядок того как мы их положим. в любом случае если плитка способна занять уровень так, что не одна другая не займёт - она займет.

      но можно найти минимальные по ширине и как-то так сделать.

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    new.contest.yandex.ru/contests/97110/problems
  49. journals.plos.org journals.plos.org
    pone.0012776 1..10
    1
    1. lucasalopz 19 Sep 2026
      When no priorknowledge is available about transcription factors, our results onthe E. coli network were however not better than random gue

      how do the results of the other models compare when there are no priors.

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    journals.plos.org/plosone/article/file
  50. www.alfredapp.com www.alfredapp.com
    Script Filter JSON Format - Alfred Help and Support
    1
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    alfredapp.com/help/workflows/inputs/script-filter/json/