GDP.pdf Benchmark
Publicación
Ver en arXivGDP.pdf: A Benchmark for Professional Document Reasoning
GDP.pdf All-pass
Costo por tarea
Tokens de salida utilizados
Puntuación
GDP.pdf: Tasa de aprobación total
GDP.pdf: Tasa de aprobación total vs. costo por tarea
Resultados por dominio
GDP.pdf: aprobación media por dominio
Costo
Los costos incluyen únicamente las llamadas al modelo participante. Se excluyen las llamadas al juez y la preparación local del PDF y el OCR.
GDP.pdf: costo por tarea
Uso de tokens
GDP.pdf: tokens de salida por tarea
Velocidad
El tiempo por tarea estima el tiempo de generación de la respuesta del participante a partir del uso de tokens de salida y la velocidad de salida del modelo. Excluye las llamadas al juez y la preparación local del PDF y el OCR.
GDP.pdf: tiempo por tarea
Tareas de ejemplo
Explora cinco tareas representativas de GDP.pdf, sus documentos de origen, entregas de modelos revisadas y las justificaciones del juez por criterio.
Instrucciones
According to the attached file, which EDS subtype(s) is associated with TNXB gene mutations and what are the differentiating characteristics of the subtype(s)?
Documento de referencia
Proporcionado al modelo
Resultado de la entrega
Una entrega de modelo revisada
Entrega del modelo
Gemini 3.5 Flash
Based on the provided research review, mutations in the TNXB gene (which encodes the tenascin-X protein) are associated with the following Ehlers-Danlos syndrome (EDS) subtypes and clinical presentations:
1. Associated EDS Subtypes
- Classical-like EDS (clEDS): Caused by autosomal recessive, biallelic mutations (homozygous or compound heterozygous) in TNXB, leading to a complete deficiency of tenascin-X (TNX).
- Contiguous Gene Syndrome (CAH-X): Caused by a contiguous gene deletion or mutation overlapping both the TNXB gene and the adjacent CYP21A2 (previously CYP21B) gene.
- TNXB Haploinsufficiency: Associated with heterozygous state mutations in TNXB that result in reduced (but not completely absent) serum TNX levels, which clinically overlaps with hypermobile EDS (hEDS).
2. Differentiating Characteristics
Classical-like EDS (clEDS)
- Primary Features: Marked by generalized joint hypermobility (GJH), soft/velvety and hyperextensible skin, and easy bruising.
- Key Differentiating Characteristics:
- Unlike classical EDS, individuals with clEDS lack the typical atrophic (papyraceous) scarring.
- It follows an autosomal recessive pattern of inheritance, whereas classical EDS is typically autosomal dominant.
CAH-X (Contiguous Gene Syndrome)
- Primary Features: Combines the connective tissue features of EDS with the endocrine features of congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency.
- Key Differentiating Characteristics:
- Patients with CAH-X exhibit significantly higher frequencies of joint hypermobility, chronic joint pain, joint dislocations, and piezogenic papules on the feet compared to patients with CAH alone.
- They are also predisposed to structural cardiac valve abnormalities.
TNXB Haploinsufficiency
- Primary Features: Present in heterozygous carriers (such as obligate family members of clEDS patients) who have roughly half of the normal level of serum TNX.
- Key Differentiating Characteristics:
- Individuals present with joint hypermobility, chronic joint pain, and joint subluxations.
- Unlike those with complete tenascin-X deficiency (clEDS), skin hyperextensibility and easy bruising are generally absent in these heterozygous individuals.
Veredictos por criterio
Resultados independientes del juez y justificaciones concisas
The answer correctly identifies classical-like EDS (clEDS) as caused by biallelic TNXB mutations leading to complete tenascin-X deficiency.
The answer correctly states that classical-like EDS results from biallelic TNXB mutations leading to a complete deficiency of tenascin-X (TNX) protein.
The answer correctly identifies TNX-deficient clEDS as caused by autosomal-recessive biallelic TNXB variants, explicitly including homozygous and compound heterozygous mutations. This satisfies the stated genetic-basis criterion.
The answer identifies generalized joint hypermobility as a primary feature of classical-like EDS (clEDS), which satisfies the criterion's required common feature.
The response explicitly lists soft/velvety skin as a primary feature of classical-like EDS (clEDS), satisfying the criterion.
The answer lists hyperextensible skin as a primary feature of classical-like EDS (clEDS), which satisfies the criterion’s required common feature.
The response explicitly lists easy bruising as a primary feature of classical-like EDS (clEDS), satisfying the criterion for a common cEDS feature.
The answer explicitly identifies TNXB haploinsufficiency as associated with heterozygous TNXB variants and states that it clinically overlaps with hypermobile EDS (hEDS), including hEDS-like features such as joint hypermobility, chronic pain, and subluxations.
The answer explicitly states that TNX-deficient classical-like EDS lacks the typical atrophic (papyraceous) scarring seen in classical EDS, directly satisfying the criterion.
The answer explicitly states that TNX-deficient classical-like EDS (clEDS) is caused by biallelic mutations and follows an autosomal recessive inheritance pattern.
The answer explicitly lists “Contiguous Gene Syndrome (CAH-X)” as a separate associated EDS subtype, contrary to the criterion requiring that CAH-X not be treated as a distinct EDS subtype.
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