「models」の検索結果

Infers person-to-person transmission from pathogen genomes using outbreaker2 (Campbell 2018), TransPhylo (Didelot 2017), phybreak (Klinkenberg 2017), BadTrIP (De Maio 2018), SCOTTI (De Maio 2016), BEASTLIER (Hall 2015), and SNP-distance / cluster-picker approaches (HIV-TRACE for HIV; transcluster). Defines outbreak clusters using pathogen-specific SNP thresholds (NOT a universal cutoff -- TB <=12 SNPs / Walker 2013; MRSA <=15 / Coll 2017; C. difficile <=2 / Eyre 2013; Klebsiella <=21 / Snitkin 2012), models within-host diversity and transmission bottlenecks (Worby-Lipsitch-Hanage 2014; McCrone 2018; Sobel Leonard 2017; Lythgoe 2021 SARS-CoV-2), integrates contact-tracing data, distinguishes generation interval from serial interval (Britton & Scalia Tomba 2019; Ali 2020), attributes source via Bayesian source attribution (Mather 2013 DT104; islandR), and reconciles transmission-network reconstruction with epi metadata. Use when investigating outbreaks for who-infected-whom, defining SNP-cluster outbreak definitions, accounting for unsampled intermediates, choosing between outbreaker2 (rich epi data) and TransPhylo (genomic-only after dated phylogeny), running source attribution between host populations, calling HIV-TRACE thresholds appropriate to the local subtype, or distinguishing recent transmission from reactivation in TB / chronic HIV.

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Calculates statistical power for high-dimensional genomics experiments (bulk RNA-seq, scRNA-seq, ATAC-seq, ChIP-seq, methylation, proteomics) under negative-binomial count models using RNASeqPower, PROPER, and simulation via powsimR, distinguishing per-gene from marginal (transcriptome-wide) power, the role of mean expression and dispersion, and the sequencing-depth-versus-replicate tradeoff. Covers simulation as the honest default for overdispersed counts, FDR-aware average power versus single-test power, observed/post-hoc power as an anti-pattern, and the winner's-curse / Type-S / Type-M consequences of underpowering. Use when planning replicate number for a sequencing experiment, deciding whether to add depth or samples, choosing closed-form versus simulation power, estimating power from pilot dispersions, or justifying replication in a grant. For clinical-trial power see clinical-biostatistics/power-and-sample-size; for the inverse sample-size question see experimental-design/sample-size.

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Runs JACKS (Joint Analysis of CRISPR/Cas9 Knockout Screens; Allen et al 2019 Genome Research) which models per-sgRNA log-fold-change as the product of a treatment-dependent gene-essentiality term and a treatment-independent guide-efficacy term. Covers the Bayesian decomposition math, the hierarchical efficacy prior shared across screens performed with the same library, when JACKS outperforms MAGeCK (multi-screen joint analysis, libraries with broad efficacy variance) and when it does not (single screen, novel libraries with no prior efficacy), library-reuse efficacy transfer, downstream essentiality interpretation, and the 2.5x sample-size reduction enabled by efficacy-aware testing. Use when running multiple screens with the same library, when guide-level noise is suspected to dominate per-gene signal, when reusing published essentiality reference screens for efficacy priors, or when comparing screens performed across cell lines that share library but differ biologically.

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Cross-method decision tree for calling hits in pooled CRISPR screens. Catalogs statistical models (MAGeCK RRA, MAGeCK MLE, BAGEL2, drugZ, JACKS, Chronos, CERES), experimental designs each is built for, failure modes outside design domain, reconciliation when methods disagree, multiple-testing and effect-size thresholds, the order of operations (count -> QC -> CN-correct -> hit-call -> validate), the second-best-sgRNA conservative rule, and consensus-hit strategy. Use when choosing among MAGeCK / BAGEL2 / drugZ / JACKS / Chronos for a given design, reconciling disagreement across two or three methods on the same screen, deciding whether to require consensus, gating downstream validation by hit-confidence tier, or interpreting unstable hit lists across reruns.

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Call copy number variants with the GATK best-practices workflows — the somatic CNV pipeline (CollectReadCounts, DenoiseReadCounts with tangent normalization, ModelSegments, CallCopyRatioSegments) and the germline GATK-gCNV pipeline (DetermineGermlineContigPloidy, GermlineCNVCaller cohort/case mode, PostprocessGermlineCNVCalls). Covers panel-of-normals construction, AnnotateIntervals/FilterIntervals, allelic-count integration, and QS-based filtering. Use when integrating CNV calling into a GATK variant pipeline, calling rare germline CNVs from an exome cohort, deciding between the somatic and germline GATK workflows, or diagnosing why tangent normalization removed a real event or why gCNV output has low precision.

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Normalize read-depth copy-ratio profiles and segment them into copy-number regions using circular binary segmentation (CBS, DNAcopy), hidden Markov models, HaarSeg, and fused-lasso methods. Covers GC-content, mappability, and replication-timing (wave-artifact) bias correction, panel-of-normals/PCA denoising, diploid-baseline centering, and algorithm selection by sequencing depth and event size. Use when choosing a segmentation algorithm, correcting depth bias, diagnosing oversegmentation or a mis-centered baseline, tuning CBS or HMM parameters, or understanding why a downstream CNV caller produced fragmented or shifted segments.

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Quantify homologous recombination deficiency (HRD) from tumor copy number using the three genomic-scar metrics — loss of heterozygosity (LOH), large-scale state transitions (LST), and telomeric allelic imbalance (TAI) — with scarHRD, and via the whole-genome HRDetect and CHORD models. Covers the genomic instability score, the PARP-inhibitor clinical context, whole-genome-doubling correction, and the scar-versus-state distinction. Use when computing an HRD score for PARP-inhibitor eligibility, deriving LOH/LST/TAI scars from allele-specific copy number, deciding between scar-based and mutational-signature HRD methods, or interpreting an HRD result in a BRCA-reverted or low-purity tumor.

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Reconcile gene trees against a species tree under probabilistic models of duplication, transfer, and loss (DTL) using ALE (Szöllősi 2013 amalgamated likelihood), GeneRax (Morel 2020 ML reconciliation), AleRax (Morel 2024 co-estimation), Whale.jl (Bayesian DTL+WGD), RANGER-DTL 2 parsimony, NOTUNG, ecceTERA, and Treerecs. Use when inferring ancestral gene-family content, distinguishing duplication from horizontal transfer from differential loss, rooting deep species trees from gene-content signals (STRIDE / Williams 2017 ALE-rooting), counting DTL events per branch, refining noisy gene trees against a species tree, modeling WGD events jointly with DTL, or producing publication-grade gene-family histories for phylogenomic / comparative analyses.

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Model gene-family birth-death dynamics across a species tree using CAFE5 (Mendes et al 2020 Bioinformatics 36:5516 gamma-distributed rate categories), CAFE5-error (annotation-error-aware), Count (Csurös 2010 ancestral state reconstruction), BadiRate (Librado 2012 likelihood + parsimony), DupliPHY-Family, and ALE/AleRax (for per-family DTL; see [[gene-tree-species-tree-reconciliation]]). Test lineage-specific gene-family expansions and contractions, distinguish biological dynamics from annotation artifacts, account for assembly fragmentation, identify functional enrichment in expanded / contracted families. Use when correlating gene-family changes with phenotype evolution, ranking lineages by adaptive gene-family-rate shifts, post-WGD dosage-balance analysis, or building Birth-death models from OrthoFinder presence/absence matrices.

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Reconstruct ancestral states at internal phylogenetic nodes for sequences (PAML codeml, IQ-TREE --ancestral, GRASP, FastML), discrete traits (corHMM hidden-rate Markov, ape::ace, phytools::make.simmap stochastic mapping, BayesTraits), and continuous traits (phytools::fastAnc, geiger Brownian/OU, RPANDA). Use when designing constructs for ancestral protein resurrection, tracing trait evolution along a tree, performing stochastic character mapping, testing models of trait evolution (BM vs OU vs EB), inferring ancestral genome content via Dollo or DTL reconciliation, or quantifying ancestral-state uncertainty for downstream comparative analyses.

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Predict RBP binding from RNA sequence using deep learning models (RBPNet sequence-to-signal, RNAProt RNN, GraphProt2 GCN with structure, DeepCLIP, DeepRiPe multi-modal CNN) for variant-effect prediction, in silico binding-site discovery, model interpretation, and transfer learning from CLIP and RBNS datasets. Use when computational prediction of RBP binding from sequence is needed, evaluating variant effects on binding without further wet-lab experiments, comparing model performance, or training a custom model on ENCODE eCLIP data.

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Performs gene-level association from GWAS summary statistics via genetically predicted tissue expression using FUSION, PrediXcan, S-PrediXcan, S-MultiXcan, UTMOST, MOSTWAS, kTWAS, EpiXcan, TIGAR-V2, and probabilistic fine-mapping with FOCUS and MA-FOCUS. Use when running TWAS from GWAS sumstats, prioritising candidate causal genes from a GWAS lead locus, picking single-tissue vs cross-tissue models, identifying LD-induced TWAS false positives, choosing ancestry-matched prediction weights, fine-mapping co-regulated TWAS hits, or triangulating TWAS with cis-eQTL Mendelian randomization and colocalization to nominate a causal gene.

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Builds and applies 3D pharmacophore models using RDKit Pharm3D, the apo2ph4 receptor-based workflow (Heider et al 2022/2023 J Chem Inf Model 63:147-158), Pharmer / Pharmit (search), and PharmacoForge (diffusion-based generation, Flynn et al 2025 Front Bioinform), covering ligand-based pharmacophore (from active set alignment) and receptor-based pharmacophore (from binding pocket geometry). Explicit handling of feature types, geometric tolerances, partial matching, and pharmacophore-based virtual screening. Use when identifying scaffold-hopping candidates, building shape-and-feature search queries, or transferring SAR across chemotypes.

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Discovers de novo motifs and tests known motif enrichment in ChIP-seq, ATAC-seq, or other peak sequences using HOMER, MEME-ChIP (STREME, CentriMo, TOMTOM, FIMO), monaLisa, and AME. Handles background selection (GC-matched, dinucleotide-shuffled, Markov order-2, peak-flanks), motif databases (JASPAR 2024 CORE PWMs, JASPAR 2026 deep-learning collection, HOCOMOCO v12, HOMER built-in), centrally-enriched motif testing, and differential motif analysis. Use when identifying TF binding motifs in peaks, testing for known TF enrichment, scanning for motif instances, comparing motif content between conditions, or interpreting motifs from deep learning models.

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Designs Bayesian clinical trials including Phase I dose-finding (BOIN, CRM, EWOC, mTPI-2), meta-analytic-predictive (MAP) priors with robust mixtures for external data borrowing, EXNEX for basket trials, hierarchical models for safety AE (Berry-Berry), Bayesian platform trials (I-SPY 2, GBM AGILE, REMAP-CAP), and posterior probability stopping rules. Covers FDA Bayesian Devices Guidance (2010), FDA Bayesian Methodology in Drugs Draft (January 2026), BOIN Fit-for-Purpose qualification (December 2021), and Project Optimus dose-optimisation. Use when designing dose-finding studies, platform trials, or sensitivity analyses with informative priors.

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Sequence-based deep learning for ATAC-seq using chromBPNet, BPNet, scBasset, or EnFormer. Use when correcting Tn5 bias with neural networks beyond k-mer models, predicting per-base accessibility profiles, scoring in silico variant effects at GWAS or rare-variant SNPs, discovering motifs via DeepLIFT/TF-MoDISco from a trained model, or generating cell-type-specific accessibility predictions for unobserved cell states.

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Harden LLM and agent integrations you operate: prompt injection, tool allowlists, secret leakage, and supply-chain of models. Defensive only.

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Enforces Pydantic v2 strict models, asynchronous dependency generators, and uv environment setup.

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Use when working with domain models, aggregates, value objects, domain events, or repositories in a DDD-style project. Ensures rich domain model over anemic CRUD.

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Picks the model a coding agent uses when a test or browser check sends an AI call. Use when choosing a model for any test, UI check, bench, or agent run, or when a test names Opus, Sonnet, Fable, Astra, or any model by habit.

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Build reactive, type-safe, production-grade backends. ALWAYS use this skill when the user asks to build, plan, design, or implement backend features, APIs, data models, server logic, database schemas, web apps, full stack apps, or mobile apps. This includes planning and architecture discussions.

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This skill should be used when the user asks to "model agent mental states", "implement BDI architecture", "create belief-desire-intention models", "transform RDF to beliefs", "build cognitive agent", or mentions BDI ontology, mental state modeling, rational agency, or neuro-symbolic AI integration.

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Expert patterns for Azure Functions development including isolated worker model, Durable Functions orchestration, cold start optimization, and production patterns. Covers .NET, Python, and Node.js programming models.

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Azure Machine Learning SDK v2 for Python. Use for ML workspaces, jobs, models, datasets, compute, and pipelines.

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