Case#: a 2‐year‐old white girl who was found to have RCM following an evaluation precipitated by the sudden death of her older brother.

DiseaseAssertion: Restrictive cardiomyopathy

FamilyInfo: 4‐year‐old brother presented with a sudden cardiac arrest while running on a soccer field and could not be resuscitated. Her father had restrictive physiology and arrhythmias. The TNNT2 variant was found in the father and two children

ParentalTesting: Father carried the variant. For both paternal grandparents tested negative and the proband inherited the variant from her father.

CasePresentingHPOs: HP:0001723, HP:0001639, HP:0031295, HP:0030718, HP:0001695

CaseHPOFreeText: "Her ECG demonstrated criteria for right and left atrial enlargement with marked repolarization abnormality. Echocardiogram revealed mild right atrial and severe left atrial enlargement (left atrial volume, 61.5 cc/m2; normal, 16–28), with mildly increased left ventricular mass and otherwise normal ventricular dimensions. Right and left ventricular systolic function was preserved. "

CaseNotHPOs: not reported

CaseNotHPOFreeText: Ventricular dimensions and biventricular systolic function were reported as normal.

CasePreviousTesting: Cardiomyopathy‐based panel testing (Familion; Transgenomic, Inc., New Haven, CT) was conducted on the proband, demonstrating a single, heterozygous, variant TNNT2‐R94C (c.280C>T).

Genotyping Method: Clinical genetic testing was performed on family members using the same HCM panel test.

FunctionalAnalysis: Biophysical experiments using recombinant human TNNT2‐R94C demonstrated impaired cardiac regulation at the molecular level attributed to reduced calcium‐dependent blocking of myosin's interaction with the thin filament.

Variant: c.835C>T, p.Gln279Ter

ClinVar: 165549

CAID: CA004288

gnomAD: not reported

AdditionalInfo: not reported

PMID: 32098556

Gene: TNNT2

HGNC ID: 11949

PMID: 37108997

Gene: TNNT2

HGNC ID: 11949

Case#: Male half-brother with mild left ventricular dilation from early childhood and mild left ventricular impairment; latest reported ejection fraction was 51%.

DiseaseAssertion: DCM

FamilyInfo: several of the siblings DCM, two died at age of 12, father had DCM, and heart transplant for an individual who later died

ParentalTesting: father was an obligate carrier

CasePresentingHPOs: HP:0001644

CaseHPOFreeText: Mild left ventricular dilation and mildly increased LV volumes

CaseNotHPOs: not reported

CaseNotHPOFreeText: not reported

CasePreviousTesting: panel-based genetic test was conducted in the index patient.

Genotyping Method: panel-based genetic test was conducted in the index patient. sanger confirmation

FunctionalAnalysis: not reported

Variant: c.659_661del p.(Lys220del)

ClinVar: 43659

CAID: CA006429

gnomAD: not reported

AdditionalInfo: not reported

Case#: A 2-year-old girl with dilated cardiomyopathy (DCM) and left ventricular noncompaction, who received a heart transplant at 26 months.

DiseaseAssertion: DCM with left ventricular noncompaction

FamilyInfo: Family history revealed that three of the father’s (A.II.2) sisters (A.II.4-A.II.6) died in infancy due to cardiac failure.

ParentalTesting: The father and paternal grandmother tested positive for the same TNNT2 variant

CasePresentingHPOs: HP:0001644, HP:0030682, HP:0001635

CaseHPOFreeText: The heart failure signs began at 2 months and got worse. Then got a heart transplant at 26 months.

CaseNotHPOs: not reported

CaseNotHPOFreeText: nothing found

CasePreviousTesting: a genetic panel test, including the genes LDB3, LMNA, MYH7, MYBPC3, and TNNT2, was performed.

Genotyping Method: Variants were confirmed in first-degree family members by Sanger sequencing.

FunctionalAnalysis: not reported

Variant: c.316G>A (p.Glu106Lys)

ClinVar: 224775

CAID: CA088557

gnomAD: not reported

AdditionalInfo: not reported

PMID: 34066613

GENE: TNNT2

HGNC ID: 11949

Case#: 19-year-old boy with coarctation of the aorta who complained of mild exertional dyspnea.

DiseaseAssertion: dilated cardiomyopathy (DCMP). LV systolic dysfunction.

FamilyInfo: The family history was positive to sudden death (his cousin died, aged 3 months) and to DCMP and heart transplant (HT): a maternal aunt and her son who then died at 42 and 24 years old. Cascade family screening revealed a TNNT2 variant in the mother (II.1) and his cousin (IV.3).

ParentalTesting: The 19 year old brother's was tested and carried the TNNT2 variant. She was also affected by DCM. The father’s testing status was not reported.

CasePresentingHPOs: HP:0001680, HP:0002875, HP:0025169, HP:4000141

CaseHPOFreeText: surgically repaired coarctation of the aorta who complained of mild exertional dyspnea repaired at birth (NYHA class II–III). Cardiac MRI showed a moderately dilated, hypokinetic LV with an ejection fraction of 45%; echocardiography showed an ejection fraction around 42%.

CaseNotHPOs: not reported

CaseNotHPOFreeText: Nothing was found that was correlated.

CasePreviousTesting: genetic investigations through next generation sequencing (NGS) with a panel of 325 genes, known to be associated with cardiomyopathies

Genotyping Method: targeted next generation sequencing

FunctionalAnalysis: not reported

Variant: c.518G>A (p. Arg173Gln)

ClinVar: 43649

CAID: CA004727

gnomAD: not reported

AdditionalInfo: not reported

PMID: 37626566

Gene: TNNT2

HGNC ID: 11949

Case#: a 20-year-old, female, adopted Indian patient with over 662 Mb regions of homozy-gosity who presented with intellectual disability, ataxia, schizophrenia, retinal dystrophy, moder-ate-to-severe progressive sensorineural hearing loss (SNHL), congenital hypothyroidism, cleft mi-tral valve with mild mitral valve regurgitation, and dysmorphic features.

DiseaseAssertion: a cleft mitral valve with mild regurgitation

FamilyInfo: adopted

ParentalTesting: not reported

CasePresentingHPOs: HP:0001249, HP:0001251, HP:0100753, HP:0000556, HP:0000407, HP:0000851, HP:0001633, HP:0001653

CaseHPOFreeText: cleft mitral valve and dysmorphic features

CaseNotHPOs: HP:0001638

CaseNotHPOFreeText: echocardiograms at 18 were normal

CasePreviousTesting: genetic testing, including targeted panel analysis, exome sequencing on a clinical basis, and a research-based review of her raw clinical exome data, led to identifying at least three causal gene disorders to explain distinct aspects of her complex phenotype.

Genotyping Method: Genome-wide single-nucleotide polymorphism (SNP) microarray analysis was clinically performed, with no pathogenic deletions or duplications detected.

FunctionalAnalysis: not reported

Variant: NM_001001430.2:c.68-1592

ClinVar: not reported

CAID: CA032911

gnomAD: total allele frequency: 0.00004522

AdditionalInfo: n/r

Case#: A 50-year-old man diagnosed with HCM at age 41, with asymmetric septal hypertrophy and exertional chest discomfort and pain

DiseaseAssertion: Hypertrophic cardiomyopathy

FamilyInfo: His third elder sister, niece and daughter were also clinically affected by HCM. The proband's mother and eldest sister had suffered from sudden cardiac death. The proband's father, second elder sister (HCM1 in Fig. 1A), nephew (HCM5 in Fig. 1A) and son (HCM7 in Fig. 1A) were 87, 65, 35, and 14 years old, respectively, and had normal echocardiographic measurements.

ParentalTesting: The mother had died suddenly; the 87-year-old father had normal echocardiographic measurements. There was no testing reported.

CasePresentingHPOs: HP:0001639, HP:0005144, HP:0100749, HP:0011712

CaseHPOFreeText: chest distress and chest pain during exercise for 9 years. He presented with an asymmetric hypertrophic interventricular septum and a maximum interventricular septum thickness of 18.04 mm

CaseNotHPOs: not reported

CaseNotHPOFreeText: no findings found in the proband

CasePreviousTesting: nothing reported in the article

Genotyping Method: hole exome sequencing (WES) Exons were captured using Sure Select Human All Exon V5 kit. Sequenced by Illumina HiSeq 4000 sequencer.

FunctionalAnalysis: not reported

Variant: rs796925245 (g.1:201359630G>A, c.835C>T, p.Gln279Ter) (c.835C>T, p.Gln279Ter)

ClinVar: 1175037

CAID: CA088451

gnomAD: not reported

AdditionalInfo: n/r

PMID: 32846832

Gene: TNNT2

HGNC ID: 11949

PMID: 21135372

Gene: TNNT2

HGNC ID: 11949

PMID:30565988

Gene:TNNT2

HGNC ID:11949

Case#:A 65-year-old woman with severe hypertrophic cardiomyopathy

DiseaseAssertion:Severe hypertrophic cardiomyopathy

FamilyInfo:no information reported

ParentalTesting:no parental testing reported

CasePresentingHPOs:HP:0001639

CaseHPOFreeText: gene panel testing that identified a single variant

CaseNotHPOs: not found

CaseNotHPOFreeText: not found

CasePreviousTesting: gene panel testing that identified a single variant

Genotyping Method:clinical gene panel testing

FunctionalAnalysis: rapid insertion of TNNT2 gene variants into induced pluripotent stem cell-differentiated cardiomyocytes (iPSC-CMs) for functional annotation of the variants for (E251D)(Figure B)

Variant:c.753G>T (p.Glu251Asp)

ClinVar:not found

CAID:CA090003

gnomAD:not found

AdditionalInfo:not reported

PMID:41969674

Gene:TNNT2

HGNC ID:11949

Case#:male, 41, DCM

DiseaseAssertion:dilated cardiomyopathy

FamilyInfo:The proband reported that his mother died suddenly at approximately 35 years of age (specific cause unknown). Other family members were healthy with no history of cardiac disease. Written informed consent was obtained from all participants.

ParentalTesting:no parental testing reported. Sanger sequencing of available family members (daughter, half-brother, maternal uncle and maternal aunt) confirmed that none carried the variant, supporting its de novo origin

CasePresentingHPOs:HP:0002875, HP:0001644, HP:4000141, HP:6000313

CaseHPOFreeText: ECG showed sinus bradycardia, occasional atrial premature beats, delayed atrioventricular conduction, left atrial enlargement, left ventricular high voltage, incomplete right bundle branch block, and ST-T changes (Figure 1C). CMR revealed late gadolinium enhancement (LGE) in the basal to mid-septal and anterolateral segments of the left ventricle (Figure 1D).

CaseNotHPOs:HP:0000822, HP:0003077

CaseNotHPOFreeText:He denied a history of hyperlipidemia, hypertension, or substance abuse.

CasePreviousTesting:No reports of previous testing

Genotyping Method:whole-exome sequencing and Sanger sequencing

FunctionalAnalysis:not reported

Variant:c.547C>T p.Arg183Trp

ClinVar:43628

CAID:CA004294

gnomAD:Overall allele frequency: 0.000001239

AdditionalInfo:not reported

PMID: 41726140

Gene: MYBPC3

HGNC ID: 7551

Case#:a 40-year-old woman with a history of hypokinetic-dilative cardiomyopathy and heterozygous for TNNT2 gene mutation

DiseaseAssertion:hypokinetic-dilative cardiomyopathy

FamilyInfo: her family appreciated the clear communication, and as her condition improved without further complications, she expressed gratitude for the care provided.

ParentalTesting:n/r

CasePresentingHPOs:HP:0001644, HP:0002094, HP:0002094, HP:0001695,

CaseHPOFreeText:Progressive dyspnea and fatigue began in January 2017. In February 2018, the patient had cardiac arrest due to ventricular fibrillation at 26 weeks’ gestation, followed by emergency caesarean section. She carried a heterozygous TNNT2 variant (c.547C>T, p.Arg183Trp)

CaseNotHPOs: HP:0031972, HP:0031972

CaseNotHPOFreeText:Coronary angiography showed no significant stenosis.

CasePreviousTesting:Testing method and scope

GenotypingMethod:n/a

FunctionalAnalysis:not reported

Variant: c.547C>T p.Arg183Trp)

Clinvar:not known

CAID:CA391630526

gnomAD:n/r

AdditionalInfo:n/r

PMID:39905734

Gene:TNNT2

HGNC ID:11949

Case#: a 50‐year‐old male who was clinically diagnosed with isolated CS and prescribed with prednisolone without much effect, and subsequent genetic analysis revealed pathogenic variants in LMNA and TNNT2, representative genes for cardiomyopathy.

DiseaseAssertion:Dilated cardiomyopathy

FamilyInfo: not reported

ParentalTesting: He had no family history of heart disease or sudden death

CasePresentingHPOs:HP:0002094,HP:0005110,HP:0025169, HP:0005110

CaseHPOFreeText:Progressive cardiac conduction disease: first-degree AV block with left axis deviation on an earlier ECG progressed to high-grade and then complete AV block. At age 50, the patient also had mild dyspnoea on exertion (New York Class ll) and atrial fibrillation. The authors later stated that it was dilated cardiomyopathy.

CaseNotHPOs:HP:0033608,HP:0002716

CaseNotHPOFreeText:CT showed no enlarged lymph nodes, pulmonary nodules, or other organ abnormalities

CasePreviousTesting: whole‐exome sequencing analysis to evaluate the risk of inherited cardiomyopathies and identified two missense variants in TNNT2 (chr1:201364335(hg38), NM_001001430.3, c.422G>A, p.Arg141Gln) and LMNA (chr1:156136096(hg38), NM_170707.4, c.1132A>C, p.Lys378Gln) (Figure 3). Sanger sequencing analysis identified a heterozygous single‐base substitution (c.1132A>C) in the LMNA gene and c.422G>A in the TNNT2 gene (red arrows).

Genotyping Method:Whole-exome sequencing (WES) identified the variants; Sanger sequencing of the TNNT2 and LMNA variants is shown in Figure 3.

FunctionalAnalysis:Not reported

Variant:TNNT2: NM_001001430.3:c.422G>A (p.Arg141Gln),LMNA: NM_170707.4:c.1132A>C (p.Lys378Gln)

ClinVar:43637

CAID:CA004540

gnomAD:not reported

AdditionalInfo:not reported

PMID:20973921

Gene:TNNT2

HGNC ID:11949

Case#:A 70‐year‐old woman, previously healthy with a left ventricular ejection fraction presented with DCM

DiseaseAssertion:dilated cardiomyopathy and a 4-month history of progressive heart failure

FamilyInfo:"Family history was negative for IDC or heart failure (Figure 3), although an uncle (II‐3) reportedly had an enlarged heart, and three other relatives (II‐1, II‐2, and III‐4) had cardiac related deaths confirmed by death certificate. The proband’s father (II‐1) died of myocardial failure and pulmonary edema; her mother (II‐2) died of pulmonary embolism; and her sister (III‐4) died suddenly of coronary artery disease in her 60s. Her daughter, the proband’s niece (IV‐3), had a history of palpitations and lower extremity swelling, intermittent numbness, and blanching of the fingers at age 49. Her echocardiogram was normal. Her ECG showed nonspecific ST‐T wave changes and left anterior hemiblock."

ParentalTesting:no parental testing reported because both parents were deceased. The two offsprings that were reported were tested and carried both variants.

CasePresentingHPOs:HP:0001644, HP:0001635, HP:0002875, HP:0012378

CaseHPOFreeText:symptoms of progressive dyspnea on exertion and fatigue that began 2–3 months prior to her presentation. Also, she had an unrelenting progression of symptoms and was hospitalized with advanced NYHA Class IV heart failure 6 weeks later. Lastly, she received a heart transplant.

CaseNotHPOs:not reported

CaseNotHPOFreeText:no myocarditis or infiltrative process and no histological evidence of hemochromatosis,

CasePreviousTesting:Oligonucleotide hybridization‐based DNA sequencing was conducted in the proband for a panel of 19 DCM genes ( Table 1 )

Genotyping Method:Oligonucleotide hybridization‐based DNA sequencing and genomic DNA was extracted from whole blood and was sequenced in our laboratory in both directions to detect and/or confirm nucleotide variants in TNNT2 in the proband and the proband’s relatives using an Applied Biosystems 3130XL capillary sequencer

FunctionalAnalysis:R139H (Figure 4): Functional studies in porcine cardiac skinned fibers reconstituted with the mutant R139H troponin T protein showed decreased Ca2+ sensitivity at pH 7, characteristic of DCM.

Variant:416G>A (R139H) in exon 10 and 690–6G>A in intron 13.

ClinVar:not found

CAID:CA004513

gnomAD:not found

AdditionalInfo:not reported

California 2026: Live Midterm Election Results - The New York Times<br /> by [[The New York Times]]<br /> accessed on 2026-11-04T21:43:41

A novel ACTC1 mutation in a young boy with left ventricular noncompaction and arrhythmias PMID: 28491642

Gene: ACTC1

HGNC ID: 143

A novel ACTC1 mutation in a young boy with left ventricular noncompaction and arrhythmias PMID: 28491642

Gene: ACTC1

HGNC ID: 143

III-1, Female 10 years old

disease assertion: VWD

**positive family history **

Parental Genotype: each has heterozygous, 3251G>A

CasePresentingHPOs: CaseHPOFreeText: BS 4, VWF Ag:0.38, *VWF:GPIbM:0.15,VWF:CB:0.13, VWFpp :0.76, FVIII:C:0.10

CaseNOTHPOs:* N.a.

CaseNOTHPOFreeText: n.a.

CasePreviousTesting: *GenotypingMethod: Sanger seqencing;

*PreviouslyPublished:n.a.

Gene:VWF Variant:c.3251G>A*

*HGVS:NM_000552.5:c.3251G>A

• *ClinVarID:Variation ID: 626952

*CAID:n.a.

*gnomAD:n.a.

Learn what a cricket betting ID is, how cricket betting accounts work, account security tips, and important legal considerations before using online services.

PMID: 33633436 Gene:ABCA4 HGNC:34

Case#: Family MD-0084 Proband, 7yo at onset

DiseaseAssertion: AR Stargardt

FamilyInfo:

CasePresentingHPOs:

CaseHPOFreeText: STGD diagnosed based on "bilateral central vision loss; fundus presenting with a beaten-bronze appearance and/or the presence of orange-yellow flecks in the retina from the posterior pole to the mid-periphery; fluorescein angiography showing typical dark choroid; and normal to subnormal electroretinogram (ERGs)." VA loss, VF loss, BCVA=<0.05/<0.05

CaseNotHPOs:

CaseNotHPOFreeText:

PreviouslyPublished: PMID: 16917483 (variant not found in this paper); PMID: 19959634

Variant: c.6410G>A (p.Cys2137Tyr) homozygous, found by ABCR400 + dHPLC + HRM + MLPA

ClinVar: 2202779

CAID: CA341277358

SupplementalData:

This variant is found in table S2A to have an OR of infinity with a CI (25.35-infinity), so PS4 is applicable

PMID:18854780

Gene: ABCA4

HGNC ID: 78

Disease: Stargardt

PMID: 19352439

Gene: ABCA4

HGNC ID: 34

Performed a meta-analysis of all data published on the rs2710102 CNTNAP2 variant up to 2015, and included Anney et al, 2012 (PMID: 20663923), Toma et al., 2013 (PMID: 23277129), Sampath et al, 2013 (PMID: 24147096), Poot et al., 2014 (PMID: 25337070 ), plus there current cohort.

No significant increase in cases vs controls for CNTNAP2 rs2710102

While this data does help support Contradictory evidence for CNTNAP2 involvement in autism, the lack of reporting of the total number of controls, as well as the number of cases and controls with the SNP prevents me from curating this information within the ClinGen gene curation interface.

Performed a meta-analysis of all data published on the rs7794745 CNTNAP2 variant up to 2015, and included Arking et al., 2008 (PMID:18179894), Li et al 2010 (PMID: 20414140), Anney et al, 2012 (PMID: 20663923), Toma et al., 2013 (PMID: 23277129), Sampath et al, 2013 (PMID: 24147096), plus there current cohort.

No significant increase in cases vs controls for CNTNAP2 rs7794745

Genotyped for the two common SNPs in CNTNAP2 rs2710102 rs7794745

CaseControlLabel: Toma 2013 CNTNAP2 rs7794745 analysis

CaseCohortLabel: 322 Autism patients

ControlCohortLabel: 524 controls

CaseCohortDisease: MONDO:0005260 (Autism)

CaseCohortPhenotype:

CaseCohortPhenotypesFreeText: Authors indicate that all individuals fulfilled DSM-IV criteria for autism or Asperger disorder. Additionally, some cases included where diagnosed with pervasive developmental disorder they may or may not have been characterized based on ADI-R and ADOS-G.

CaseControlNOTPhenotype:

CaseControlNOTPhenotypeFreeText:

CaseDemographics: 269 men, 53 women, Average age= = 17y.o. of Spanish and/or Caucasian descent.

ControlDemographics: controls were noted to be sex-matched and unrelated, however no numbers or ages were indicated. Sample obtained from the Blood and Tissues Bank of Hospital Universitari Vali d'Hebron.

CaseGenotypingMethod: One SNP, rs7794745, was genotyped using PCR-RFLP, from DNA obtained from peripheral blood lymphocytes (salting out method).

ControlGenotypingMethod: One SNP, rs7794745, was genotyped using PCR-RFLP, from DNA obtained from peripheral blood lymphocytes (salting out method).

CasePower: 312/322

ControlPower: 505/524

CaseAddInfo: Other genetic variation is not noted.

ControlAddInfo: Other genetic variation is not noted.

CaseControlStudyType: Single Variant Analysis

CaseControlDetectionMethod: Cases and controls genotyped for single variant

CaseControlStats: p-value= 0.87

CaseControlBias: Cases and controls are ethinically matched, and noted to be sex-matched.

CaseControlComments:

Case:9 months old male DiseaseAssertion:Infantile neuroaxonal dystrophy FamilyInfo:Paternally inherited mutation CasePresentingHPOs:HP:0002376,HP:0000648,HP:0000648,HP:0012444 Case HPO Free Text: N/A Case NOT HPOs: N/A Genotyping Method: Targeted Sanger sequencing identified PLA2G6 mutations c.[1799G>A];[2221C>T] . Both mutations have previously been identified in unrelated patients with PLAN. Variant:NM_003560.2:c.2221C>T ClinVarID:265448 gnomAD:https://gnomad.broadinstitute.org/variant/22-38112559-G-A?dataset=gnomad_r4 Multiple Gene Variants: GeneName:PLA2G6 Variant:NM_003560.2:c.1799G>A ClinVarID:159748 gnomAD:https://gnomad.broadinstitute.org/variant/22-38116155-C-T?dataset=gnomad_r4

this is showing how fast television became popular in the U.S. after WWII. once broadcasting started in 1947, almost everyone wanted a TV, and within a few years most households had one

what were some of the key court cases that helped challenge antiblack laws, especially in education?

this is saying that racism in the South wasn’t just social, it was also built into laws and everyday customs but change started happening through court cases, especially around education, where people began challenging those unfair laws.

this part is explaining how the government and banks basically worked together to create segregation in housing. they used these maps to label neighborhoods by risk, but really it was based on race, since areas with minorities were marked as dangerous

How did shifting gender norms create tension between younger women and older generations during this period?

How did the “Lost Cause” help white southerners justify white supremacy and reshape the South’s image to the rest of the nation?

Why do you think people in 1878 were willing to believe that technology could completely end hunger and poverty?

The economic state of the world affected the emotions of Americans. Economic depression.

Who funded this? was it the government or was it the tax payers?

The amount of violence endured just for the right to protest.

what would happen to the farmers who stood up against this or united to fight the injustices? Was there any organizations?

• The methods of analyzing a work is more important than whether or not it is considered literary
• Texts that were excluded from the canon tend to be argued into the literary canon via such analysis

PMID: 34209044 Gene: MYH6, NKX2-5 HGNC ID: 7576, 2488

PMID:28302740 Gene: GATA4, NKX2-5 HGNC ID: 4173, 2488

PMID: 35182466 Gene: GATA4 HGNC ID: 4173

PMID: 37123967 Gene: GATA4 HGNC: 4173

PMID:36263775 Gene: GATA4 HGNC ID:4173

Google Learns training data 10/25

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Specialized LLMs - specialized data sets

5 takeaways from Tuesday's elections, including bad news for Elon Musk by [[Domenico Montanaro]]

Reply to Hajo Bakker on LinkedIn

Hajo Bakker Exam vs. Test -- Een examinering moet veel vanafwegen en niet regulier gebeuren.

Een test (toets) mag vaker gebeuren, en moet weinig vanaf hangen... Geen ouders die straffen voor een laag cijfer (of cijfers afschaffen), geen adviezen die daarvanafhangen, etc.

Het doel van een toets is om je aan te geven wat je krachten en minder sterke punten zijn, dus waar je je op moet focussen met toekomst leren. Dit kan alleen op het moment dat je een toets nabespreekt en op individueel niveau. Klassikaal bespreken heeft vaak weinig nut.

Daarbij komt ook dat een student moet snappen WAAROM het helpt om na te bespreken, de wetenschap erachter. Op het moment dat je de waarom achter het hoe niet goed snapt heeft het hoe minder effect. (dit is waarom in het 4C/ID model ze in een scaffold beginnen met de laatste stap, waarin de informatie van voorgaande stappen is gegeven. Dit zodat als je de vorige stap gaat leren, je een beter idee hebt waar het uiteindelijk voor gebruikt gaat worden en je er dus een betere invulling aan kan geven.)

Semantische verschillen zijn vaak uiterst nuttig om complexe stof te begrijpen. Op het moment dat ze exact hetzelfde waren heeft het weinig nut om meerdere termen te hebben en zouden ze synoniem zijn.

"Exam" is geen synoniem van "test".

Genuanceerde verschillen zijn vaak nuttiger dan "umbrella terms" om goed te communiceren, als uiterst subliem wordt beargumenteerd in "Science of Memory: Concepts" van Roediger III et al.

Daarnaast komt uiteraard bij kijken dat neurocognitieve wetenschap een blauwdruk geeft voor hoe onze brein architectuur in elkaar zit (zie bijvoorbeeld John Sweller, Cognitive Load Theory 2011, en The Forgetting Machine, Rodrigo Quian Quiroga, 2017, Science of Memory: Concepts, Roediger et al., 2007, Ten Steps to Complex Learning, van Merriënboer, 2017).

Dit is universeel toepasbaar, afgezien van mensen met een cognitieve aandoening bijvoorbeeld, dit gaat dus over neurotypische breinen.

Leerstijlen zijn een mythe, wel hebben wij leervoorkeuren, maar door alleen in onze leervoorkeur te leren missen wij bepaalde informatie die cruciaal kan zijn voor beter begrip en meesterschap (mastery).

Beter is het om studietechnieken te gebruiken die overeenkomen met brein-architectuur en die onder te knie te krijgen.

Meer cognitieve belasting te gebruiken (zonder cognitieve overbelasting te veroorzaken). Als leren "makkelijk" voelt is het over het algemeen niet uitdagend genoeg en/of de techniek niet nuttig. Herlezen / samenvatten is simpel maar vrij inefficiënt. Het maken van een GRINDEmap voelt moeilijk maar is vele malen effectiever (zie ook the misinterpreted effort hypothesis).

Zoals Dr. Ahrens al zei: "The one who does the effort, does the learning."

Verder heb ik een heleboel ideëen voor een optimaal onderwijs dat zich aanpast aan het individu in plaats van aan het systeem, maar dit is een te complex en groot onderwerp om zo even hier neer te zetten.

Reply to Gertina Blanket on LinkedIn:

Jij legt in één klap uit datgene wat ik nooit goed heb begrepen uit de literatuur... Het verschil tussen interleaving en varied practice (die vaak als hetzelfde worden gebruikt in de "volksmond").

Het een gaat over verschillende hoeken kijken naar hetzelfde idee (varied practice) terwijl het ander gaat over verschillende maar soortgelijke ideëen (interleaving), bijvoorbeeld meerdere soorten wiskunde (algebra, trigonometrie, etc.).

Hierbij wil ik uiteraard wel zeggen dat blocked practice niet per se direct toegepast moet worden als het over automatisering gaat -- de cognitieve schemata moeten eerst goed gevormd zijn. Zie ook 4C/ID (Ten Steps to Complex Learning). Ofwel, eerst goede encoding + retrieval (Spaced Interleaved Retrieval, mindmapping, etc.) en dan focus op "drilling" / knowledge fluency.

Het sneller maken / automatiseren heeft geen enkel nut als het begrip er nog niet goed in zit. Dit moet geverifiëerd worden.

Kennis is natuurlijk ook erg interdisciplinair. Ik wordt er extreem blij van als ik een link leg tussen een boek over filosofie en efficiënt leren/onderwijs bijvoorbeeld.

Zo las ik ooit een boek over romeinse oratoren met een misleidende titel "How to Win an Argument" van Marcus Tullius Cicero, vertaald door James M. May, en hierin kwam ik tegen dat de oude Romeinen al door hadden dat LOGICA is wat het brein doet onthouden, en dit hoeft dus geen objective logica te zijn maar meer een correcte reflectie van hoe je eigen geest werkt en verbanden legt.

Dit is direct in lijn met wat ik weet van cognitieve leerpsychologie en mijn klein beetje kennis van neurowetenschap (waar ik dit jaar dieper in wil duiken).

Informatie in isolatie is nooit stevig, het moet zich vastklampen aan ankers en andere kennis (voorkennis eventueel), en de lerende (niet de onderwijzende) moet actief bezig zijn om deze verbanden te leggen.

Zoals ik wel vaker quote van Dr. Sönke Ahrens: "The one who does the effort does the learning."

Als ik een boek lees denk ik automatisch aan hoe ik dit kan relateren aan wat al in mijn second mind (Zettelkasten) zit. Ik denk niet meer linear, alleen maar non-linear. Standaard in verbanden.

Hier wat bronnen (impliciet) genoemd: - Cicero, M. T. (2016). How to win an argument: An ancient guide to the art of persuasion (J. M. May, Trans.). Princeton University Press. - Ahrens, S. (2017). How to take smart notes: One simple technique to boost writing, learning and thinking: for students, academics and nonfiction book writers. CreateSpace. - fast, sascha. (100 C.E., 45:02). English Translation of All Notes on Zettelkasten by Luhmann. Zettelkasten Method. https://zettelkasten.de/posts/luhmanns-zettel-translated/ - Luhmann, N. (1981a). Communicating with Slip Boxes (M. Kuehn, Trans.). 11. - Luhmann, N. (1981b). Kommunikation mit Zettelkästen. In H. Baier, H. M. Kepplinger, & K. Reumann (Eds.), Öffentliche Meinung und sozialer Wandel / Public Opinion and Social Change (pp. 222–228). VS Verlag für Sozialwissenschaften. https://doi.org/10.1007/978-3-322-87749-9_19 - Moeller, H.-G. (2012). The radical Luhmann. Columbia University Press. - Scheper, S. (2022). Antinet Zettelkasten: A Knowledge System That Will Turn You Into a Prolific Reader, Researcher and Writer. Greenlamp, LLC.

• Schmidt, J. F. K. (2016). Niklas Luhmann’s Card Index: Thinking Tool, Communication Partner, Publication Machine. In Forgetting Machines: Knowledge Management Evolution in Early Modern Europe (pp. 287–311). Brill. https://doi.org/10.1163/9789004325258_014
• Schmidt, J. F. K. (2018). Niklas Luhmann’s Card Index: The Fabrication of Serendipity. Sociologica, 12(1), Article 1. https://doi.org/10.6092/issn.1971-8853/8350

This section of the text describes how someone's last thoughts when dying affect the future they will have. It implies that their final thoughts have an impact on how they live in the future, suggesting an idea of the afterlife. The Gita reinforces concepts of karma and rebirth by highlighting the value of dedication and focus. Krishna makes this point in the lesson by referring to Arjuna as "Kunti’s Son," encouraging him to keep his attention on the divine as a way to attain ultimate freedom.

Effect: He likes beer, likely an alcoholic Motif: Angels

Effect: He's abnormal, creature-like Motif: Angels

In another ceremony, I have been shown that there is a parasite in our limbic systems - I was told that some people know it s ID (Jung)

for - AI music - youtube content ID algorithms can identify it

I thought things are content-addressed. Having a string name is strange.

The main idea, able to be generalized, I get from this video is that in order to develop any skill, whether it is learning or something else, you need to break it down into its constituents, much like the 4 Component Instruction Design model argues, and figure out where your weak links are.

The more accurately you know the system of your skill, the better you know what to potentially improve on. This requires research, and sometimes asking experts.

Another benefit of networking.

I.e., linking by non-content-based id is not BFT.

I.e., giving nodes IDs that are not content-based is not BFT strategy.

What stops him?

Would be nice to have truly unique ids. E.g., a public key.

Eats more space, but can be zipped over the wire. Given there are many ops transferred.

Also could be possible to create pubkey -> int mapping per-document, so it's damm more compact. That would require consensus on this map.

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The Green Knight shows his excitement to take the hit from Sir Gawain's hand in response to his wanting to take on the challenge. This implies a feeling of loyalty and willingness to carry out their end of the bargain. But then the Green Knight secretly changes the terms of the first agreement struck with King Arthur by adding a new condition to their agreement. The Green Knight adds a sense of mystery as well as potential risk for Gawain when he asks him to vow on his honor to find him later and offer a prize equal to the one he received today.

Greek plays are either tragedies or comedies. There is a much deeper meaning to them than just entertaining the public. Keeping this in mind when reading the stories gives them a much deeper meaning.(https://www.worldhistory.org/Greek_Theatre/) To know the full extent of what they were really meant for is important to the readers. For this specific play, the meaning behind the story is that the men in charge are operating from an excessively limited perspective as they ignore their partners' informed advice. This is a huge political controversy to this day. Women are very overlooked in society especially considering how far back this is dated. Back when this play was written women were given tasks like cooking and cleaning and had little to no rights so this was a good political example of how they were treated and overlooked.

0 1 2 3 0 1 2 3 4 5 6 7 8 9 0 1 2 3 4 5 6 7 8 9 0 1 2 3 4 5 6 7 8 9 0 1 +-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+ | unix_ts_ms | +-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+ | unix_ts_ms | ver | rand_a | +-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+ |var| rand_b | +-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+ | rand_b | +-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+

https://research.vu.nl/en/publications/on-the-impact-of-sameas-on-schema-matching

```python def split_user(userid): """ Return the user and domain parts from the given user id as a dict.

For example if userid is u'acct:seanh@hypothes.is' then return
{'username': u'seanh', 'domain': u'hypothes.is'}'

:raises InvalidUserId: if the given userid isn't a valid userid

"""
match = re.match(r"^acct:([^@]+)@(.*)$", userid)
if match:
    return {"username": match.groups()[0], "domain": match.groups()[1]}
raise InvalidUserId(userid)

```

Wow, you can't create an Apple ID without assigning yourself a telephone tracking number.

Incredible.