「lia」の検索結果

Comprehensive quality control for CLIP-seq libraries (eCLIP, iCLIP, iCLIP2, PAR-CLIP) covering library complexity (preseq), FRiP, IDR replicate reproducibility, read-distribution metagene, SMInput vs IgG control rationale, rRNA / snoRNA contamination, fragment-length distribution, and ENCODE-compliance thresholds. Use when assessing whether a CLIP library passed, deciding lenient vs stringent peak thresholds, comparing replicates with IDR rescue and self-consistency ratios, or distinguishing failed IP from over-amplified library.

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Identify direct miRNA-target interactions from AGO HITS-CLIP, AGO-CLEAR-CLIP (chimeric reads), HEAP (Halo-Ago2 mouse), chimeric eCLIP / miR-eCLIP (deep miRNA-target profiling), or CLASH using chimeric-read processing pipelines, seed-pairing analysis, and 3' auxiliary pairing rules. Use when distinguishing direct miRNA targets from indirect, integrating CLIP-derived target maps with TargetScan / miRDB / DIANA predictions, applying canonical 7mer-8mer seed matching with 3' UTR context, or recovering miRNA-mRNA chimeras at scale.

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Prioritizes rare-disease variants from trio/quad WES/WGS with de novo (DeNovoGear, Triodenovo), compound-heterozygous phasing (WhatsHap), mosaic VAF tiering, phenotype-driven ranking (Exomiser, Phen2Gene, AMELIE), ClinGen gene-disease validity gating, and ACMG SF v3.2 secondary findings reporting. Use when running diagnostic exome / genome pipelines, identifying candidate Mendelian disease genes, screening for incidental findings, or auditing VUS reclassification cycles. The ACMG/AMP classification framework (PVS1 decision tree, Pejaver PP3/BP4 calibration, Tavtigian point system) is in clinical-databases/acmg-classification.

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Infer orthologous genes and gene families across species using OrthoFinder3 (HOG-based phylogenetic orthology), SonicParanoid2, Broccoli, ProteinOrtho, OMA / FastOMA hierarchical orthologous groups, eggNOG-mapper, JustOrthologs, and TOGA whole-genome-alignment orthology. Use when building single-copy ortholog sets for phylogenomics, classifying co-orthologs and in/out-paralogs after gene duplication, propagating functional annotation via orthology with awareness of the ortholog conjecture, distinguishing speciation from duplication via gene-tree species-tree reconciliation, computing Quest-for-Orthologs benchmark performance, or running synteny-aware ortholog detection in WGD-affected lineages.

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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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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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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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Runs cis-pQTL Mendelian randomization for drug-target validation using UKB-PPP (Olink), deCODE (SomaScan), Fenland, INTERVAL, ARIC, and FinnGen-PPP proteomes plus colocalization triangulation, phenome-wide on-target adverse-effect scans, cross-platform Olink/SomaScan replication, and PAV (protein-altering variant) sensitivity. Use when nominating or de-risking a drug target from plasma-proteome GWAS, mimicking pharmacological inhibition via cis-pQTL instruments, separating shared-causal from LD-confounded signal under the Schmidt 2020 cis-MR framework, screening on-target adverse phenotypes pheWAS-style, or producing publication-grade STROBE-MR plus PP.H4 evidence for a target gene.

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Detect and adjust for horizontal pleiotropy in two-sample Mendelian randomization by distinguishing uncorrelated (UHP) from correlated (CHP) pleiotropy and choosing among Egger, MR-PRESSO, MR-RAPS, CAUSE, LHC-MR, LCV, MR-Clust, MR-Mix, and contamination-mixture methods. Use when validating an MR causal claim, running the STROBE-MR sensitivity battery, suspecting a shared heritable confounder, working under weak-instrument or polygenic-exposure regimes, or reconciling discordant estimates across robust methods.

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Calls HLA class I and class II alleles at 2/4/6/8-field resolution from WGS/WES/RNA-seq/long-read data using OptiType, HLA-LA, T1K, Polysolver, HLA-HD, arcasHLA, StarPhase, or HIBAG imputation. Use when typing for HSCT, solid-organ transplant, neoantigen prediction, PGx screening (B*57:01, B*15:02, etc.), or disease-association studies, with reconciliation across tools and IPD-IMGT/HLA version mismatch handling.

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Estimates bivariate genetic correlation (rg) between traits from GWAS summary statistics or individual-level genotypes using cross-trait LDSC, HDL, LAVA, rho-HESS, GREML-bivariate, Popcorn, and HDL-L. Use when quantifying shared genetic architecture between two traits, screening MR validity before causal inference, distinguishing global from locus-level rg, estimating trans-ancestry rg, separating partial from full causation via LCV gcp, or producing a STROBE-MR-compliant cross-trait sensitivity battery. Cross-trait LDSC intercept absorbs sample overlap and is NOT a bias; HDL is biased under sample overlap above ~5%. High rg between exposure and outcome motivates CHP-aware MR sensitivity (CAUSE, LHC-MR).

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Trim multiple sequence alignments using ClipKIT, trimAl, BMGE, Divvier, or HMMcleaner with mode selection guidance per downstream goal. Use when removing unreliable columns or contaminating residues before phylogenetic inference, HMM building, or selection analysis.

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Use this skill when working with Brain Imaging Data Structure (BIDS) datasets: organizing neuroscience and biomedical data (MRI, EEG, MEG, iEEG, PET, microscopy, NIRS, motion capture, EMG, MR spectroscopy, behavioral), querying BIDS layouts, validating compliance, converting DICOM to BIDS, writing metadata sidecars, or creating BIDS derivatives.

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Agile product ownership toolkit for Senior Product Owner including INVEST-compliant user story generation, sprint planning, backlog management, and velocity tracking. Use for story writing, sprint planning, stakeholder communication, and agile ceremonies.

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This skill determines whether testicular volume should be used as the primary or sole indicator of sexual development in male childhood cancer survivors who have received gonadotoxic treatments such as alkylating agents or testicular radiotherapy. Triggers include clinician questions like “Can I use testicular volume to assess puberty in this male survivor after chemotherapy?” or “Is testis size reliable for sexual maturity evaluation post‑radiation?”

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Determines if a patient has completed ≥1 year of consistent and compliant hormone therapy for genital surgery approval. Triggers include patient requesting genital surgery and being on hormone therapy.

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Determines when to test for germline KCNJ5 mutations indicating familial hyperaldosteronism type III in very young patients with primary aldosteronism. Triggered by severe early-onset hypertension with hypokalemia in infants or young children (<20 years) with confirmed PA.

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Recommends using mineralocorticoid receptor antagonists rather than epithelial sodium-channel inhibitors for medical treatment of primary aldosteronism. Use when a clinician asks whether to use an MRA or ENaC inhibitor for medical treatment of PA.

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Suggests using prednisolone 3–5 mg/d orally once or twice daily as a glucocorticoid alternative in primary adrenal insufficiency. Consider this option when evaluating glucocorticoid therapy, particularly in patients with reduced medication compliance.

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Interprets the postural stimulation test to detect angiotensin II‑unresponsive aldosterone‑producing adenoma (APA) or familial hyperaldosteronism type I (FH‑I) when aldosterone fails to rise with upright posture. Triggered by clinical cues such as “postural stimulation test shows no aldosterone increase”, “suspected APA with non‑responsive aldosterone”, or “evaluating FH‑I in young patients with early‑onset hypertension and hypokalemia”.

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Order and interpret lipoprotein(a) [Lp(a)] measurement at least once in a lifetime, apply the risk-enhancer threshold (≥125 nmol/L or ≥50 mg/dL), and run cascade screening of first-degree relatives for premature ASCVD, familial hypercholesterolaemia, or elevated Lp(a) per the 2026 ACC/AHA multisociety dyslipidaemia guideline. Covers the Class 1 lifetime measurement, how elevated Lp(a) affects LLT initiation and intensification, the cascade screening indications, the interaction of Lp(a) with ASCVD risk estimation, and current therapeutic limitations. Use when a clinician asks when to check Lp(a), how often to repeat Lp(a), elevated Lp(a) what next, treatment for high Lp(a), should I screen my patient's family, Lp(a) and statins, cascade screening indications. Grounded in the 2026 ACC/AHA multisociety dyslipidaemia guideline.

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Tell the agent to zoom out and give broader context or a higher-level perspective. Use when you're unfamiliar with a section of code or need to understand how it fits into the bigger picture.

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Subjects every non-trivial decision to a fresh-context adversarial review before it stands. Use when correctness matters more than speed, when working in unfamiliar code, when stakes are high (production, security-sensitive logic, irreversible operations), or any time a confident output would be cheaper to verify now than to debug later.

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Autonomous agents are AI systems that can independently decompose goals, plan actions, execute tools, and self-correct without constant human guidance. The challenge isn't making them capable - it's making them reliable. Every extra decision multiplies failure probability.

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