. * * window.aa needs to exist and be usable by ANY module's script, * however early it runs - main-nav's script, for one, runs near * the top of

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, well before the real search-insights.js * so the download * begins as early as before. Repeat calls share the same downloads, a * failed load is retried on the next call, and the versions / SRI * hashes live only here. * * Algolia Insights is unaffected: window.aa above is still created in * on every page and queues events until search-insights loads. * * window.loadAlgoliaLibs({ priority: 'high' }) (Oct 2026): used by the * /search page, where the first results wait on these libraries. Chrome * gives async scripts low priority, behind images and fonts; this asks * for high instead (fetchpriority). Only the first call for a library * sets its priority - later calls share that download. */ (function (win, doc) { var LIBS = [ { ready: function () { return !!win['algoliasearch/lite']; }, src: 'https://cdn.jsdelivr.net/npm/algoliasearch@5.52.1/dist/lite/builds/browser.umd.js', integrity: 'sha256-I2oYUIvhx1g6l4lTP+yoERbzLIHKzw4AKaBRQPwIeDY=' }, { ready: function () { return !!win.instantsearch; }, src: 'https://cdn.jsdelivr.net/npm/instantsearch.js@4.98.0/dist/instantsearch.production.min.js', integrity: 'sha256-ngmqZk4WBxUw257aMYZayyNBd983INngagv0jI6Ecfs=' } ]; function loadOne(lib, options) { if (lib.ready()) return Promise.resolve(); // One download per library, shared by every caller; reset on // failure so the next call retries just the library that failed. if (lib.pending) return lib.pending; lib.pending = new Promise(function (resolve, reject) { var script = doc.createElement('script'); script.src = lib.src; script.integrity = lib.integrity; script.crossOrigin = 'anonymous'; script.async = true; if (options && options.priority === 'high') script.setAttribute('fetchpriority', 'high'); script.onload = function () { lib.ready() ? resolve() : reject(new Error('Loaded but not available: ' + lib.src)); }; script.onerror = function () { script.remove(); reject(new Error('Could not load ' + lib.src)); }; doc.head.appendChild(script); }); lib.pending.catch(function () { lib.pending = null; }); return lib.pending; } win.loadAlgoliaLibs = function (options) { return Promise.all(LIBS.map(function (lib) { return loadOne(lib, options); })); }; })(window, document); . */ window.hsConversationsSettings = window.hsConversationsSettings || {}; window.hsConversationsSettings.loadImmediately = false; (function (win) { var EVENTS = ['pointerdown', 'keydown', 'touchstart', 'scroll', 'mousemove', 'wheel']; var done = false; /* 19 Oct 2026 - chat widget layout shift (field CLS). Phones fail Core Web Vitals on CLS (p75 ~0.2 site-wide in CrUX for months). Biggest cause found: HubSpot's chat container is fixed to the bottom-right corner and changes size - 100x96 launcher to 282x253 when the welcome message pops up (~5 s after load), and to full screen when a visitor opens the chat. Its top-left corner moves, so Chrome scores it as a layout shift: 0.088 per page view at 360x640 (0.044 at 412x850), on every page. Taps happen inside the chat iframe, so the parent page never sees the input and the open/close shifts count too. Fix: whenever the container's size changes it is made transparent for 400 ms (Chrome doesn't score shifts of invisible elements), then shown again at its new size. Tested on live io1001 at 360x640 in a cookie-less frame: the 0.088 shift no longer appears. The chat itself is unchanged - it just appears 0.4 s later at each resize. Relies on HubSpot's container id; if that changes this does nothing (no error). */ function cloakChatResizes() { var ID = 'hubspot-messages-iframe-container'; function watch(c) { if (c.getAttribute('data-bb-cloak')) return; c.setAttribute('data-bb-cloak', '1'); var last = c.offsetWidth + 'x' + c.offsetHeight, timer = null; new MutationObserver(function () { var size = c.offsetWidth + 'x' + c.offsetHeight; if (size === last) return; last = size; c.style.setProperty('opacity', '0', 'important'); clearTimeout(timer); timer = setTimeout(function () { c.style.removeProperty('opacity'); }, 400); }).observe(c, { attributes: true, attributeFilter: ['style', 'class'], subtree: true, childList: true }); } var found = document.getElementById(ID); if (found) { watch(found); return; } if (!document.body || !('MutationObserver' in win)) return; var mo = new MutationObserver(function () { var c = document.getElementById(ID); if (c) { mo.disconnect(); watch(c); } }); mo.observe(document.body, { childList: true }); setTimeout(function () { mo.disconnect(); }, 30000); } function loadWidget() { var api = win.HubSpotConversations; if (api && api.widget && api.widget.status && api.widget.status().loaded) return; try { cloakChatResizes(); } catch (e) {} if (api && api.widget) api.widget.load(); } function onFirstInteraction() { if (done) return; done = true; EVENTS.forEach(function (type) { win.removeEventListener(type, onFirstInteraction, { passive: true }); }); var start = function () { if (win.HubSpotConversations) loadWidget(); else (win.hsConversationsOnReady = win.hsConversationsOnReady || []).push(loadWidget); }; if ('requestIdleCallback' in win) win.requestIdleCallback(start, { timeout: 1500 }); else setTimeout(start, 200); } EVENTS.forEach(function (type) { win.addEventListener(type, onFirstInteraction, { passive: true }); }); })(window);

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Optical pooled CRISPR screen in iPSC-derived human ioMicroglia using Element Biosciences AVITI24 system
Poster

Optical pooled CRISPR screen in iPSC-derived human ioMicroglia using Element Biosciences AVITI24 system

Targets with human genetic evidence are twice as likely to succeed in clinical trials and gain drug approval compared to those without (Nelson et al., Nature Genetics, 2015). Identifying and validating such targets requires systematic approaches that can connect genetic perturbations to complex cellular phenotypes in physiologically relevant models.

You will learn:

  • How CRISPRko-Ready ioMicroglia combined with the Element Biosciences enable simultaneous in situ detection of sgRNA identity, protein abundance and cell morphology in a single experiment

  • How optical sgRNA detection recovered distinct perturbation identities across spatially distributed, morphologically heterogeneous cells, with library representation and target coverage comparable to conventional pooled CRISPR screens and a median of 109 cells per perturbation in each polarisation state

  • How protein and morphology profiling discriminates M0, M1- and M2-like microglia states, and how HDAC3, DOT1L and PRMT6 knockouts shift microglia away from the M1 state, consistent with an essential role for these genes in maintaining it

Perlova et al

In collaboration with Element Biosciences and VBCF NGS Facility

2026

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