「pert」の検索結果

Designs novel molecules using REINVENT 4 (de novo, scaffold decoration, linker design, R-group, molecular optimization), MolMIM, Diffusion-based generators (DiGress, DiffSMol), and JT-VAE with explicit handling of multi-parameter optimization (MPO), goal-directed scoring functions, transfer/reinforcement/curriculum learning, synthetic accessibility scoring, and chemical space exploration vs exploitation. Use when designing new chemical matter against a target, decorating a scaffold, linking fragments, or optimizing a hit for multiple ADMET / activity properties simultaneously.

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Designs and analyzes combinatorial CRISPR screens covering paired-Cas9 (Big Papi, Najm 2018), enhanced AsCas12a multiplex (enCas12a, DeWeirdt 2021), in4mer 4-guide-array Cas12a (Esmaeili Anvar N et al 2024 Nat Commun 15:3577) and the Inzolia paralog-pair library, paralog-buffering detection (Dede 2020 Genome Biol; Thompson 2021 Nat Commun 12:1302), genetic-interaction (GI) scoring as observed_double_LFC minus expected_additive_double_LFC, synthetic-lethal and synthetic-rescue interaction interpretation, the half-of-essentiality buffered by paralogs phenomenon, multiplex screen statistical analysis with MAGeCK MLE interaction terms, and the relationship to single-cell combinatorial Perturb-seq. Use when designing a paralog or pathway-pair screen, choosing between paired-Cas9 (Big Papi) and Cas12a multiplex (Inzolia), interpreting genetic interaction scores, identifying synthetic-lethal targets for drug development, or scaling beyond single-gene CRISPR screens.

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Profiles RNA-binding protein targets without antibody or UV crosslinking using STAMP (APOBEC1-RBP fusion, C-to-U editing), scSTAMP (single-cell), TRIBE/HyperTRIBE (ADAR-RBP, A-to-I editing), DART-seq (APOBEC1-YTH for m6A), or Bullseye/SAILOR edit-site detection pipelines. Use when antibody is unavailable or specificity is doubtful, when single-cell RBP profiling is needed (scSTAMP), or when in vivo RBP profiling without UV is preferred.

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Predicts ADMET properties using ADMETlab 3.0 (119 platform features, including 77 prediction models with modeled-endpoint uncertainty), ADMET-AI, DeepChem MolNet, and chemprop D-MPNN with explicit handling of OECD QSAR principles, applicability domain assessment, calibration, hERG/CYP/AMES endpoints, and PAINS / Lipinski / Ro5 / Veber / BBB druglikeness filters. Use when filtering compounds for drug-likeness, prioritizing leads by predicted safety, or building an in-house ADMET QSAR model.

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Expert guide for Backend.AI distributed computing platform. Automatically activates when users ask about: - Backend.AI architecture, components (Manager, Agent, Storage Proxy, Webserver, App Proxy) - Features (session scheduling, Sokovan orchestrator, multi-tenancy, resource allocation) - APIs (REST, GraphQL), authentication, RBAC authorization - Container runtime (kernels, jail sandbox, hook library, virtual folders) - Accelerator support (CUDA, ROCm, TPU, NPU, Graphcore IPU) - Client SDKs (Python, Java, JavaScript, PHP) - Setup, requirements (Python 3.13+, Docker, PostgreSQL, Redis, etcd) - How WebUI connects to/interacts with Backend.AI backend - Plugin interfaces, development setup, infrastructure Use when user mentions "Backend.AI", "backend.ai", "Sokovan", component names, or asks about the backend platform this WebUI connects to. allowed-tools: WebFetch, Read

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AWS serverless and event-driven architecture expert based on Well-Architected Framework. Use when building serverless APIs, Lambda functions, REST APIs, microservices, or async workflows. Covers Lambda with TypeScript/Python, API Gateway (REST/HTTP), DynamoDB, Step Functions, EventBridge, SQS, SNS, and serverless patterns. Essential when user mentions serverless, Lambda, API Gateway, event-driven, async processing, queues, pub/sub, or wants to build scalable serverless applications with AWS best practices.

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AWS Cloud Development Kit (CDK) expert for building cloud infrastructure with TypeScript/Python. Use when creating CDK stacks, defining CDK constructs, implementing infrastructure as code, or when the user mentions CDK, CloudFormation, IaC, cdk synth, cdk deploy, or wants to define AWS infrastructure programmatically. Covers CDK app structure, construct patterns, stack composition, and deployment workflows.

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Analyze a single FASTA file (nucleotide or protein), compute sequence-level metrics (GC, ORFs, MW, pI, GRAVY, secondary-structure fractions) with Biopython, and write a Markdown report plus structured JSON for downstream chaining.

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Transition insulin pump to scheduled subcutaneous basal bolus insulin when anticipated hospital length of stay exceeds 1 to 2 days and pump expertise is unavailable. Triggers include: "Patient expected to stay >2 days, should we switch pump to scheduled insulin?

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Apply the four published expert-consensus clinical scenarios to manage GI adverse events in complex GLP-1 receptor agonist patients — persistent nausea mid-titration, GERD/heartburn after up-titration, elderly with sarcopenia risk, and insulin-treated elderly with CKD plus diarrhoea. Use when a clinician describes a patient resembling one of these archetypes, or asks "how to manage GLP-1 in an elderly patient with CKD", "patient on liraglutide developed reflux", "sarcopenia worry on semaglutide in 80-year-old", or "persistent nausea on semaglutide despite escalation". Grounded in Gorgojo-Martínez 2023 Table 4.

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This skill evaluates infusion site health and rotates sites appropriately to prevent lipohypertrophy or infection. It is triggered when clinicians inspect pump sites for irritation or lumps or review site rotation practice at visit.

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This skill directs lifelong treatment of cardiovascular risk factors, osteoporosis, and psychiatric symptoms in all patients with Cushing's syndrome until biochemical resolution of hypercortisolism. Use when managing any CS patient for long‑term comorbidity control; triggers include persistent hypertension, dyslipidemia, low bone density, depression, anxiety, or cognitive changes in the setting of known or suspected CS.

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This skill recommends that all patients with Cushing’s syndrome receive monitoring and adjunctive treatment for cortisol-dependent comorbidities including psychiatric disorders, diabetes, hypertension, hypokalemia, infections, dyslipidemia, osteoporosis, and poor physical fitness. Apply when managing any CS patient to address associated health issues; triggers include confirmed or suspected hypercortisolism, preoperative evaluation, postoperative follow‑up, or persistent hypercortisolism despite treatment.

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This skill recommends using biochemical tests to screen for hypercortisolism to detect recurrence in patients with ACTH-dependent Cushing's syndrome after surgical remission. It is triggered during postoperative follow-up when the HPA axis has recovered, annually, or sooner if clinical signs of hypercortisolism (e.g., weight gain, hypertension, glucose intolerance) or abnormal late-night salivary cortisol/UFC appear.

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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 switching specific anti-hypertensive medications to reduce false-positive and false-negative screening results for primary aldosteronism. Triggered when a clinician notes 'The patient is on ACE inhibitors/ARBs' or suspects medication interference with screening results.

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Suggests considering mineralocorticoid receptor antagonists when benefits outweigh risks in pregnant or preconception PA patients with uncontrolled hypertension and hypokalemia. Triggered when standard therapy fails and clinicians ask 'Should I consider MRAs despite pregnancy?' or when assessing risk‑benefit of MRA use.

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Provides evidence-based guidelines for preoperative optimization and postoperative monitoring in patients with primary aldosteronism undergoing adrenalectomy. Triggers include when planning surgery or starting treatment and asking 'What perioperative care is needed?' or managing complications such as resistant hypertension, hypokalemia, or suspected cortisol co-secretion.

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Determines when to avoid aldosterone suppression testing in hypertensive patients with a positive PA screen who have normokalemia and suppressed aldosterone below assay‑specific cutoffs (<11 ng/dL immunoassay or <8 ng/dL LC‑MS/MS), indicating low likelihood of primary aldosteronism. Use when a clinician asks whether to skip confirmatory suppression testing based on low pretest probability.

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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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Calculates the lowest effective glucocorticoid dose (dexamethasone or prednisone) to normalize blood pressure and serum potassium in glucocorticoid-remediable aldosteronism (GRA/FH-I) by titrating to biochemical and clinical targets. Indicated when initiating medical treatment for confirmed GRA, triggered by findings such as early-onset hypertension, family history of stroke before age 40, spontaneous hypokalemia, or suppressed plasma renin activity with elevated aldosterone.

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Suggests that pregnant patients with primary adrenal insufficiency be monitored for clinical signs of glucocorticoid over- or under-replacement such as normal weight or gain, fatigue, postural hypotension or hypertension, and hyperglycemia, with at least one review each trimester. Use when managing a pregnant patient with PAI to assess glucocorticoid dosing adequacy.

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Interprets the saline infusion test (SIT) to assess the probability of primary aldosteronism when a patient has a positive aldosterone-to-renin ratio (ARR) and requires confirmatory testing. Triggers include evaluating post‑infusion plasma aldosterone concentration (PAC) after a positive ARR, hypertension work‑up, or when deciding whether to proceed to adrenal venous sampling (AVS).

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Determines whether to add a mineralocorticoid receptor antagonist (e.g., spironolactone or eplerenone) to glucocorticoid therapy in glucocorticoid-remediable aldosteronism when blood pressure fails to normalize with glucocorticoid alone. Triggered by persistent hypertension or inadequate BP control despite optimized glucocorticoid dosing in GRA patients.

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